category mir disease pmid root_name doid icd10cm mesh omim hpo description genetics_GWAS hsa-mir-146a Acute Cerebral Infarction 23202363 cardiovascular system disease DOID:3526 I63 D002544 Association of the miR-146a, miR-149, miR-196a2, and miR-499 Polymorphisms With Ischemic Stroke and Silent Brain Infarction Risk genetics_GWAS hsa-mir-149 Acute Cerebral Infarction 23202363 cardiovascular system disease DOID:3526 I63 D002544 Association of the miR-146a, miR-149, miR-196a2, and miR-499 Polymorphisms With Ischemic Stroke and Silent Brain Infarction Risk genetics_GWAS hsa-mir-196a-1 Acute Cerebral Infarction 23202363 cardiovascular system disease DOID:3526 I63 D002544 Association of the miR-146a, miR-149, miR-196a2, and miR-499 Polymorphisms With Ischemic Stroke and Silent Brain Infarction Risk genetics_GWAS hsa-mir-196a-2 Acute Cerebral Infarction 23202363 cardiovascular system disease DOID:3526 I63 D002544 Association of the miR-146a, miR-149, miR-196a2, and miR-499 Polymorphisms With Ischemic Stroke and Silent Brain Infarction Risk genetics_GWAS hsa-mir-146a Acute Coronary Syndrome 26537765 I24.9 D054058 These findings indicate that miR-146a rs2910164 may act as a novel molecular marker for ACS susceptibility. genetics_GWAS hsa-mir-107 Adenocarcinoma, Gastric 25771723 disease of cellular proliferation DOID:3717 D37.1 D013274 miR-107 is dysregulated in GAC pathogenesis and the SNP rs2296616 may play a role in the process. genetics_GWAS hsa-mir-199a Adenocarcinoma, Pancreatic Ductal 26872370 disease of cellular proliferation DOID:3498 C25.3 D021441 260350 our study demonstrates that host genetic variants could disturb the regulation of the miR-199a/HIF1A regulatory loop and alter PDAC risk and poor prognosis. genetics_GWAS hsa-mir-146a Alcohol Use Disorder 24630744 disease of mental health DOID:1574 F10.1 D000437 This is the first genetic association study to explore the relationship of miRNA polymorphisms with AUDs and to show an association of the miR-146a C>G rs2910164 allelic variant with this disease. genetics_GWAS hsa-mir-149 Allergic Rhinitis 28181414 respiratory system disease DOID:4481 J30.9 D065631 607154 HP:0003193 A functional variant of miRNA-149 confers risk for allergic rhinitis and comorbid asthma in Chinese children. genetics_GWAS hsa-mir-146a Alzheimer Disease 24586483 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 A functional polymorphism in the promoter region of microRNA-146a is associated with the risk of Alzheimer disease and the rate of cognitive decline in patients. genetics_GWAS hsa-mir-146a Alzheimer Disease 26095531 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 A single nucleotide polymorphism in primary-microRNA-146a reduces the expression of mature microRNA-146a in patients with Alzheimer's disease and is associated with the pathogenesis of Alzheimer's disease. genetics_GWAS hsa-mir-146a Ankylosing Spondylitis 25836258 musculoskeletal system disease DOID:7147 M45.9 D013167 Association between ankylosing spondylitis and the miR-146a and miR-499 polymorphisms. genetics_GWAS hsa-mir-499 Ankylosing Spondylitis 25836258 musculoskeletal system disease DOID:7147 M45.9 D013167 Association between ankylosing spondylitis and the miR-146a and miR-499 polymorphisms. genetics_GWAS hsa-mir-128 Anxiety Disorders 19370765 disease of mental health DOID:2030 F41.9 D001008 607834 HP:0000739 Allele variants in functional MicroRNA target sites of the neurotrophin-3 receptor gene (NTRK3) as susceptibility factors for anxiety disorders. genetics_GWAS hsa-mir-148a Anxiety Disorders 19370765 disease of mental health DOID:2030 F41.9 D001008 607834 HP:0000739 Allele variants in functional MicroRNA target sites of the neurotrophin-3 receptor gene (NTRK3) as susceptibility factors for anxiety disorders. genetics_GWAS hsa-mir-148b Anxiety Disorders 19370765 disease of mental health DOID:2030 F41.9 D001008 607834 HP:0000739 Allele variants in functional MicroRNA target sites of the neurotrophin-3 receptor gene (NTRK3) as susceptibility factors for anxiety disorders. genetics_GWAS hsa-mir-152 Anxiety Disorders 19370765 disease of mental health DOID:2030 F41.9 D001008 607834 HP:0000739 Allele variants in functional MicroRNA target sites of the neurotrophin-3 receptor gene (NTRK3) as susceptibility factors for anxiety disorders. genetics_GWAS hsa-mir-485 Anxiety Disorders 19370765 disease of mental health DOID:2030 F41.9 D001008 607834 HP:0000739 Allele variants in functional MicroRNA target sites of the neurotrophin-3 receptor gene (NTRK3) as susceptibility factors for anxiety disorders. genetics_GWAS hsa-mir-509 Anxiety Disorders 19370765 disease of mental health DOID:2030 F41.9 D001008 607834 HP:0000739 Allele variants in functional MicroRNA target sites of the neurotrophin-3 receptor gene (NTRK3) as susceptibility factors for anxiety disorders. genetics_GWAS hsa-mir-765 Anxiety Disorders 19370765 disease of mental health DOID:2030 F41.9 D001008 607834 HP:0000739 Allele variants in functional MicroRNA target sites of the neurotrophin-3 receptor gene (NTRK3) as susceptibility factors for anxiety disorders. genetics_GWAS hsa-mir-146a Arthritis 25269878 musculoskeletal system disease DOID:848 M19.90 D001168 This meta-analysis suggests that the miR-499 rs374644 and IRAKI rs3027898 polymorphisms are associated with susceptibility to inflammatory arthritis. genetics_GWAS hsa-mir-499 Arthritis 25269878 musculoskeletal system disease DOID:848 M19.90 D001168 This meta-analysis suggests that the miR-499 rs374644 and IRAKI rs3027898 polymorphisms are associated with susceptibility to inflammatory arthritis. genetics_GWAS hsa-mir-146a Asthma 22823586 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 MiR-146a polymorphism is associated with asthma but not with systemic lupus erythematosus and juvenile rheumatoid arthritis in Mexican patients. genetics_GWAS hsa-mir-146a Asthma 27431205 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 The miR鈥?46a rs2910164 polymorphism CC genotype was identified to be significantly associated with a decreased risk of BHR in response to intubation when compared with the GG or GC genotype (odds ratio, 0.38; confidence interval, 0.18鈥?.78). genetics_GWAS hsa-mir-152 Asthma 27383317 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 Single nucleotide polymorphisms in the promoter region of mir-133a-1 and in pre-mir-152 rs1707 may contribute to the risk of asthma in a Chinese Han population. genetics_GWAS hsa-mir-196a2 Asthma 27487239 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 microRNA-196a2 rs11614913 polymorphism might be associated with asthma severity in our sample of the Egyptian population. genetics_GWAS hsa-mir-146a Atherosclerosis 26875519 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Apolipoprotein E Epsilon 4 Enhances the Association between the rs2910164 Polymorphism of miR-146a and Risk of Atherosclerotic Cerebral Infarction. genetics_GWAS hsa-mir-146a Atherosclerosis 28674224 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Association of NFKB1A and microRNAs variations and the susceptibility to atherosclerosis. genetics_GWAS hsa-mir-196a2 Atrial Fibrillation 26554236 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 Our data support that the pre-miR-196a2 polymorphism is associated with AF, and the C allele is a risk factor for AF. genetics_GWAS hsa-mir-4436b-1 Autism Spectrum Disorder 24667286 disease of mental health DOID:0060041 F84.0 D000067877 209850 HP:0000729 Assessing the impact of copy number variants on miRNA genes in autism by Monte Carlo simulation. genetics_GWAS hsa-mir-4436b-2 Autism Spectrum Disorder 24667286 disease of mental health DOID:0060041 F84.0 D000067877 209850 HP:0000729 Assessing the impact of copy number variants on miRNA genes in autism by Monte Carlo simulation. genetics_GWAS hsa-mir-146a Autoimmune Diseases [unspecific] 25830862 D001327 607836 HP:0002960 MiR-146a rs2910164 G>C polymorphism was associated with the susceptibility of ADs. genetics_GWAS hsa-mir-125a Autoimmune Thyroiditis 24990808 immune system disease DOID:7188 E06.3 D013967 109100 Associations of single nucleotide polymorphisms in precursor-microRNA (miR)-125a and the expression of mature miR-125a with the development and prognosis of autoimmune thyroid diseases. genetics_GWAS hsa-mir-146a Behcet Disease 23268366 cardiovascular system disease DOID:13241 M35.2 D001528 109650 MicroRNA-146a and Ets-1 gene polymorphisms in ocular Behcet's disease and Vogt-Koyanagi-Harada syndrome genetics_GWAS hsa-mir-146a Behcet Disease 26053525 cardiovascular system disease DOID:13241 M35.2 D001528 109650 Association of Pre-miRNA-499 rs3746444 and Pre-miRNA-146a rs2910164 Polymorphisms and Susceptibility to Behcet's Disease. genetics_GWAS hsa-mir-182 Behcet Disease 24801147 cardiovascular system disease DOID:13241 M35.2 D001528 109650 Predisposition to Behcet's disease and VKH syndrome by genetic variants of miR-182. genetics_GWAS hsa-mir-499 Behcet Disease 26053525 cardiovascular system disease DOID:13241 M35.2 D001528 109650 Association of Pre-miRNA-499 rs3746444 and Pre-miRNA-146a rs2910164 Polymorphisms and Susceptibility to Behcet's Disease. genetics_GWAS hsa-mir-140 Bladder Neoplasms 26695686 C67 D001749 109800 HP:0009725 Together, these results suggest that rs35592567 in TP63 may be a novel causal variant contributing to the susceptibility to bladder cancer, which provides additional insight into the pathogenesis of bladder carcinogenesis. genetics_GWAS hsa-mir-143 Bladder Neoplasms 27438131 C67 D001749 109800 HP:0009725 These findings suggest that the functional rs353293 polymorphism may be a useful biomarker to predict the risk of bladder cancer. genetics_GWAS hsa-mir-145 Bladder Neoplasms 27438131 C67 D001749 109800 HP:0009725 These findings suggest that the functional rs353293 polymorphism may be a useful biomarker to predict the risk of bladder cancer. genetics_GWAS hsa-mir-146a Bladder Neoplasms 29491365 C67 D001749 109800 HP:0009725 miR-146a rs2910164 polymorphism is a risk factor for urological neoplasms, particularly for bladder cancer genetics_GWAS hsa-mir-21 Bladder Neoplasms 24078506 C67 D001749 109800 HP:0009725 In accordance to the observed similarity between TGF-β variants and miR-21 gene expression alterations in bladder tumors, treating 5637 bladder cancer cell line with TGF-β recombinant protein caused a significant upregulation of miR-21. The later finding further confirmed a correlated expression of TGF-βand miR-21 in bladder tumors. genetics_GWAS hsa-mir-27b Bladder Neoplasms 24312312 C67 D001749 109800 HP:0009725 Taken together, these findings suggested that DROSHA rs10719T>C polymorphism may be associated with bladder cancer risk in a Chinese population, and hsa-miR-27b can influence the expression of DROSHA protein by binding with 3'UTR. genetics_GWAS hsa-mir-101-1 Breast Neoplasms 24475105 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Genetic variations in the flanking regions of miR-101-2 are associated with increased risk of breast cancer. genetics_GWAS hsa-mir-101-2 Breast Neoplasms 24475105 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Genetic variations in the flanking regions of miR-101-2 are associated with increased risk of breast cancer. genetics_GWAS hsa-mir-103a-2 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-106b Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-1-1 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-124-1 Breast Neoplasms 21318219 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Genetic variants (SNP rs1042538 A/T) at the miR-124 binding site on the cytoskeleton-organizing IQGAP1 gene confer differential predisposition to breast cancer. genetics_GWAS hsa-mir-124-2 Breast Neoplasms 21318219 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Genetic variants (SNP rs1042538 A/T) at the miR-124 binding site on the cytoskeleton-organizing IQGAP1 gene confer differential predisposition to breast cancer. genetics_GWAS hsa-mir-124-3 Breast Neoplasms 21318219 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Genetic variants (SNP rs1042538 A/T) at the miR-124 binding site on the cytoskeleton-organizing IQGAP1 gene confer differential predisposition to breast cancer. genetics_GWAS hsa-mir-125a Breast Neoplasms 23420759 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 rs12976445 variant in the pri-miR-125a correlates with a lower level of hsa-miR-125a and ERBB2 overexpression in breast cancer patients genetics_GWAS hsa-mir-125b Breast Neoplasms 26190157 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Evaluation the susceptibility of five polymorphisms in microRNA-binding sites to female breast cancer risk in Chinese population. genetics_GWAS hsa-mir-125b Breast Neoplasms 19738052 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 A risk variant in an miR-125b binding site in BMPR1B is associated with breast cancer pathogenesis. genetics_GWAS hsa-mir-133a-2 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-135b Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-145 Breast Neoplasms 26577090 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Our study is the first to report an association between a miR-SNP in MIR145 and breast cancer risk in individuals of Caucasian background. This finding requires further validation through genotyping of larger cohorts or in individuals of different ethnicities to determine the potential significance of this finding as well as studies aimed to determine functional significance. genetics_GWAS hsa-mir-146a Breast Neoplasms 24039706 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 This meta-analysis demonstrates the compelling evidence that the rs11614913 CC genotype in miR-196a2 increases breast cancer risk, which provides useful information for the early diagnosis and prevention of breast cancer. genetics_GWAS hsa-mir-146a Breast Neoplasms 26476291 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The microRNA miR146a has a potential role in the development of breast cancer and the effects of its SNPs require further inquiry to determine the nature of their influence on breast tissue and cancer. genetics_GWAS hsa-mir-146a Breast Neoplasms 18634034 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-146: rs2910164 were associated with increased risk of breast cancer in Chinese women genetics_GWAS hsa-mir-146a Breast Neoplasms 18660546 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-146a: A functional polymorphism (rs2910164) in the miR-146a gene and age of familial breast/ovarian cancer diagnosis genetics_GWAS hsa-mir-146a Breast Neoplasms 22363415 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The authors found that hs-miR-196a2 in premenopausal patients, and hs-miR-499, hs-miR-146a and hs-miR-196a2 in postmenopausal patients, may discriminate breast cancer patients from healthy individuals. In addition, we found a significant association between two microRNA polymorphisms (hs-miR-196a2 and hs-miR-499) and breast cancer risk. genetics_GWAS hsa-mir-146a Breast Neoplasms 22363684 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Increased Risk of Breast Cancer Associated with CC Genotype of Has-miR-146a Rs2910164 Polymorphism in Europeans. genetics_GWAS hsa-mir-146a Breast Neoplasms 26785832 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 e identified one rare variant in MIR146A, four in MIR146B, five in BRCA1 3'-UTR and one in BRCA2 3'-UTR in 716 index cases and 619 controls. genetics_GWAS hsa-mir-146a Breast Neoplasms 27434289 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Logistic regression data represented the C allele of rs2910164 (OR = 4.00, p= 0.0037) as the risk allele and associated with Her2-positive phenotype. genetics_GWAS hsa-mir-146a Breast Neoplasms 29521182 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Effects of miR-27a, miR-196a2 and miR-146a polymorphisms on the risk of breast cancer genetics_GWAS hsa-mir-146b Breast Neoplasms 18634034 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-146: rs2910164 were associated with increased risk of breast cancer in Chinese women genetics_GWAS hsa-mir-146b Breast Neoplasms 26785832 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 we identified one rare variant in MIR146A, four in MIR146B, five in BRCA1 3'-UTR and one in BRCA2 3'-UTR in 716 index cases and 619 controls. genetics_GWAS hsa-mir-149 Breast Neoplasms 18634034 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-149: rs2292832 were associated with increased risk of breast cancer in Chinese women genetics_GWAS hsa-mir-151a Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-153-2 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-17 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-17 Breast Neoplasms 19048628 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-17: mutations genetics_GWAS hsa-mir-17 Breast Neoplasms 21140207 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 SNP (rs3739008) located at 3'UTR of NPAS2 and the C to T changing of the SNP may disrupt the binding of microRNA- (miR-)17-5p and miR-519e to the 3'UTR of NPAS2 genetics_GWAS hsa-mir-17 Breast Neoplasms 25680407 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Association of microRNA 17-92 cluster host gene (MIR17HG) polymorphisms with breast cancer. genetics_GWAS hsa-mir-18 Breast Neoplasms 25680407 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Association of microRNA 17-92 cluster host gene (MIR17HG) polymorphisms with breast cancer. genetics_GWAS hsa-mir-18a Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-194-1 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-196a Breast Neoplasms 24039706 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 This meta-analysis demonstrates the compelling evidence that the rs11614913 CC genotype in miR-196a2 increases breast cancer risk, which provides useful information for the early diagnosis and prevention of breast cancer. genetics_GWAS hsa-mir-196a Breast Neoplasms 24922658 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The current study provides evidence that the miR-196a rs11614913T>C polymorphisms are possible prognostic biomarker for patients with hormone receptor-expressing early breast cancer. genetics_GWAS hsa-mir-196a-1 Breast Neoplasms 23228090 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Evaluation of single nucleotide polymorphisms in microRNAs (hsa-miR-196a2 rs11614913 C/T) from Brazilian women with breast cancer genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 26125831 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Our results suggested that miR-146a rs2910164 G>C and miR-196a2 rs11614913 T>C may be biomarkers for predicting breast cancer risk in the Chinese population. genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 23982873 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the current meta-analysis supports that the miR-196a-2 rs11614913*T, miR-499 rs3746444*T, miR-605 rs2043556*A, and miR-27a rs895919*C alleles might be protective factors for breast cancer genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 26710106 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Somatic Mutation of the SNP rs11614913 and Its Association with Increased MIR 196A2 Expression in Breast Cancer. genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 18634034 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-196a-2: rs11614913 were associated with increased risk of breast cancer in Chinese women genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 21483822 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 rs11614913 polymorphism:Overall, individuals with the TC/CC genotypes were associated with higher cancer risk than those with the TT genotype (OR=1.18, 95% CI=1.03-1.34, P<0.001 for heterogeneity test). In the stratified analyses, we observed that the CC genotype might modulate breast cancer risk (OR=1.11, 95%CI=1.01-1.23, P(heterogeneity)=0.210) and lung cancer risk (OR=1.25, 95%CI=1.06-1.46, P(heterogeneity)=0.958), comparing with the TC/TT genotype. Moreover, a significantly increased risk was found among Asian populations in a dominant model (TC/CC versus TT, OR=1.24, 95% CI=1.07-1.43, P(heterogeneity)=0.006). genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 22074121 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The Chinese women with menarche age less than 16 years had increased breast cancer risk (OR = 2.10, 95% CI: 1.23-3.60). Marginally significant association between rs11614913 (hsa-miR-196a-2) CT/CC genotypes and reduced breast cancer risk was observed (OR = 0.65, 95% CI: 0.40-1.06), genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 22363415 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The authors found that hs-miR-196a2 in premenopausal patients, and hs-miR-499, hs-miR-146a and hs-miR-196a2 in postmenopausal patients, may discriminate breast cancer patients from healthy individuals. In addition, we found a significant association between two microRNA polymorphisms (hs-miR-196a2 and hs-miR-499) and breast cancer risk. genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 23228090 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Evaluation of single nucleotide polymorphisms in microRNAs (hsa-miR-196a2 rs11614913 C/T) from Brazilian women with breast cancer genetics_GWAS hsa-mir-196a-2 Breast Neoplasms 29521182 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Effects of miR-27a, miR-196a2 and miR-148a polymorphisms on the risk of breast cancer genetics_GWAS hsa-mir-199a-2 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-19a Breast Neoplasms 25680407 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Association of microRNA 17-92 cluster host gene (MIR17HG) polymorphisms with breast cancer. genetics_GWAS hsa-mir-19a Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-19b-1 Breast Neoplasms 25680407 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Association of microRNA 17-92 cluster host gene (MIR17HG) polymorphisms with breast cancer. genetics_GWAS hsa-mir-19b-1 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-200a Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-200b Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-20a Breast Neoplasms 25680407 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Association of microRNA 17-92 cluster host gene (MIR17HG) polymorphisms with breast cancer. genetics_GWAS hsa-mir-20a Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-214 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-215 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-218-1 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-219-1 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-25 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-27a Breast Neoplasms 23982873 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the current meta-analysis supports that the miR-196a-2 rs11614913*T, miR-499 rs3746444*T, miR-605 rs2043556*A, and miR-27a rs895919*C alleles might be protective factors for breast cancer genetics_GWAS hsa-mir-27a Breast Neoplasms 25556434 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 an association between pre-miR-27a polymorphism rs895819 and cancer risk in Caucasians. The protective effect of rs895819 [G] allele in younger breast cancer and in the group of unilateral breast cancer patients await further confirmation since the included studies in this meta-analysis were limited. genetics_GWAS hsa-mir-27a Breast Neoplasms 23954879 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 A genetic variant in pre-miR-27a is associated with a reduced breast cancer risk in younger Chinese population. genetics_GWAS hsa-mir-27a Breast Neoplasms 29521182 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Effects of miR-27a, miR-196a2 and miR-147a polymorphisms on the risk of breast cancer genetics_GWAS hsa-mir-296 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-302a Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-302b Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-302c Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-302d Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-30b Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-30c-1 Breast Neoplasms 19048628 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-30c-1: mutations genetics_GWAS hsa-mir-30d Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-320 Breast Neoplasms 26190157 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Evaluation the susceptibility of five polymorphisms in microRNA-binding sites to female breast cancer risk in Chinese population. genetics_GWAS hsa-mir-320a Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-338 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-339 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-367 Breast Neoplasms 26190157 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Evaluation the susceptibility of five polymorphisms in microRNA-binding sites to female breast cancer risk in Chinese population. genetics_GWAS hsa-mir-367 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-367 Breast Neoplasms 21810988 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Functional SNP (rs1044129, is present in binding region) in the microRNA-367 binding site in the 3'UTR of the calcium channel ryanodine receptor gene 3 (RYR3) affects breast cancer risk and calcification. genetics_GWAS hsa-mir-383 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number loss genetics_GWAS hsa-mir-423 Breast Neoplasms 22593246 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 A genetic variant (rs6505162:A>C) located in miR-423 is associated with reduced breast cancer risk. genetics_GWAS hsa-mir-429 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-485 Breast Neoplasms 25003827 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-485-5p binding site SNP rs8752 in HPGD gene is associated with breast cancer risk. genetics_GWAS hsa-mir-488 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-499 Breast Neoplasms 23982873 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the current meta-analysis supports that the miR-196a-2 rs11614913*T, miR-499 rs3746444*T, miR-605 rs2043556*A, and miR-27a rs895919*C alleles might be protective factors for breast cancer genetics_GWAS hsa-mir-499 Breast Neoplasms 24039706 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 This meta-analysis demonstrates the compelling evidence that the rs11614913 CC genotype in miR-196a2 increases breast cancer risk, which provides useful information for the early diagnosis and prevention of breast cancer. genetics_GWAS hsa-mir-499 Breast Neoplasms 24521023 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Our findings demonstrated that the hsa-mir-499 rs3746444 polymorphism is associated with higher risk of developing breast cancer in our population. genetics_GWAS hsa-mir-499 Breast Neoplasms 19847796 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Recently, the SNPs rs11614913 in hsa-mir-196a2 and rs3746444 in hsa-mir-499 were reported to be associated with increased breast cancer risk, and the SNP rs2910164 in hsa-mir-146a was shown to have an effect on age of breast cancer diagnosis. genetics_GWAS hsa-mir-499 Breast Neoplasms 23053947 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 In conclusion, this meta-analysis suggests that the miR-499 rs3746444 polymorphism (A>G) is a low-penetrant risk factor for cancer development among Asians and may contribute to breast cancer susceptibility. genetics_GWAS hsa-mir-499a Breast Neoplasms 18634034 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-499: rs3746444 were associated with increased risk of breast cancer in Chinese women genetics_GWAS hsa-mir-499a Breast Neoplasms 22363415 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The authors found that hs-miR-196a2 in premenopausal patients, and hs-miR-499, hs-miR-146a and hs-miR-196a2 in postmenopausal patients, may discriminate breast cancer patients from healthy individuals. In addition, we found a significant association between two microRNA polymorphisms (hs-miR-196a2 and hs-miR-499) and breast cancer risk. genetics_GWAS hsa-mir-519e Breast Neoplasms 21140207 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 SNP (rs3739008) located at 3'UTR of NPAS2 and the C to T changing of the SNP may disrupt the binding of microRNA- (miR-)17-5p and miR-519e to the 3'UTR of NPAS2 genetics_GWAS hsa-mir-603 Breast Neoplasms 26718432 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 In conclusion,the findings indicated that Mir603 rs11014002 T allele might contribute to decrease the risk of BC in a sample of Iranian population. Further studies with larger sample sizes and different ethnicities are warranted to confirm our findings. genetics_GWAS hsa-mir-605 Breast Neoplasms 23982873 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the current meta-analysis supports that the miR-196a-2 rs11614913*T, miR-499 rs3746444*T, miR-605 rs2043556*A, and miR-27a rs895919*C alleles might be protective factors for breast cancer genetics_GWAS hsa-mir-608 Breast Neoplasms 22586447 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Polymorphism rs4919510:C>G in mature sequence of human microRNA-608 contributes to the risk of HER2-positive breast cancer but not other subtypes. genetics_GWAS hsa-mir-6826 Breast Neoplasms 27380242 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 We systematically put together a list of 822 and 10,468 genetic variants among primary miRNA sequences and 38 genes in the miRNA biogenesis pathway genetics_GWAS hsa-mir-9-1 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-92-1 Breast Neoplasms 25680407 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Association of microRNA 17-92 cluster host gene (MIR17HG) polymorphisms with breast cancer. genetics_GWAS hsa-mir-92a Breast Neoplasms 26471763 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 MDM4 SNP34091 status to be associated with reduced risk of breast cancer, in particular in individuals carrying the MDM2 SNP309GG genotype, but not to be associated with either lung-, colon- or prostate cancer. genetics_GWAS hsa-mir-93 Breast Neoplasms 16754881 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 copy number gain genetics_GWAS hsa-mir-200b Carcinoma, Breast 27609814 D05 D001943 114480 HP:0003002 Mutation of putative miRNA-binding sites (miR-374a/b, miR-200b/c, miR-29a/b/c, miR-488) in these regions did not have significant impact on 3'UTR activity genetics_GWAS hsa-mir-200c Carcinoma, Breast 27609814 D05 D001943 114480 HP:0003002 Mutation of putative miRNA-binding sites (miR-374a/b, miR-200b/c, miR-29a/b/c, miR-488) in these regions did not have significant impact on 3'UTR activity genetics_GWAS hsa-mir-205 Carcinoma, Breast 27885248 D05 D001943 114480 HP:0003002 Rs3842530 Polymorphism in MicroRNA-205 Host Gene in Lung and Breast Cancer Patients. genetics_GWAS hsa-mir-29a Carcinoma, Breast 27609814 D05 D001943 114480 HP:0003002 Mutation of putative miRNA-binding sites (miR-374a/b, miR-200b/c, miR-29a/b/c, miR-488) in these regions did not have significant impact on 4'UTR activity genetics_GWAS hsa-mir-29b Carcinoma, Breast 27609814 D05 D001943 114480 HP:0003002 Mutation of putative miRNA-binding sites (miR-374a/b, miR-200b/c, miR-29a/b/c, miR-488) in these regions did not have significant impact on 5'UTR activity genetics_GWAS hsa-mir-374a Carcinoma, Breast 27609814 D05 D001943 114480 HP:0003002 Mutation of putative miRNA-binding sites (miR-374a/b, miR-200b/c, miR-29a/b/c, miR-488) in these regions did not have significant impact on 6'UTR activity genetics_GWAS hsa-mir-374b Carcinoma, Breast 27609814 D05 D001943 114480 HP:0003002 Mutation of putative miRNA-binding sites (miR-374a/b, miR-200b/c, miR-29a/b/c, miR-488) in these regions did not have significant impact on 7'UTR activity genetics_GWAS hsa-mir-488 Carcinoma, Breast 27609814 D05 D001943 114480 HP:0003002 Mutation of putative miRNA-binding sites (miR-374a/b, miR-200b/c, miR-29a/b/c, miR-488) in these regions did not have significant impact on 8'UTR activity genetics_GWAS hsa-mir-561 Carcinoma, Breast 24166930 D05 D001943 114480 HP:0003002 Genetic variant rs16430 6bp > 0bp at the microRNA-binding site in TYMS and risk of sporadic breast cancer risk in non-Hispanic white women aged ≤ 55 years. genetics_GWAS hsa-mir-627 Carcinoma, Breast 27807724 D05 D001943 114480 HP:0003002 rs15869 at miRNA binding site in BRCA2 is associated with breast cancer susceptibility. genetics_GWAS hsa-mir-124 Carcinoma, Cervical 24589598 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 miR-124 rs531564 polymorphism may play a role in cervical cancer susceptibility in Chinese Han women, and G allele is associated with a reduced risk of cervical cancer. genetics_GWAS hsa-mir-135b Carcinoma, Cervical 24465869 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 Genetic variants in microRNA target sites of 37 selected cancer-related genes and the risk of cervical cancer. genetics_GWAS hsa-mir-146a Carcinoma, Cervical 26464690 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 The miR-146a (rs2910164) polymorphism is significantly correlated to ethnic factor and tumor diameters. miR-146a has differential expression in cervical tissues. Allele G of miR-146a (rs2910164) is related to the high expression of miR-146a, and the progression of cervical cancer. genetics_GWAS hsa-mir-21 Carcinoma, Cervical 25987069 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 E6D25E of the HPV16As variant differed from the E6 prototype in its activities on epigenetic modulation and immune surveillance and this might be a key factor for the important role of this variant in cervical cancer progression. genetics_GWAS hsa-mir-27a Carcinoma, Cervical 24380734 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 A genetic variant in pre-miR-27a is associated with a reduced cervical cancer risk in southern Chinese women. genetics_GWAS hsa-mir-502 Carcinoma, Cervical 25169478 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 These data suggest that there are significant associations between the miR-502-binding site SNP in the 3'-UTR of SET8 and the TP53 codon 72 polymorphism with cervical cancer in Chinese, and there is a gene-gene interaction. genetics_GWAS hsa-let-7 Carcinoma, Colon 24727325 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 In the largest association study investigating the LCS6 polymorphism in colon cancers, the germline LCS6 genotype was not associated with KRAS mutation status or with clinical outcome in patients with stage III tumors. genetics_GWAS hsa-let-7a Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-143 Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-145 Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-146a Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-146a Carcinoma, Colon 27706637 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 MicroRNA variants and colorectal cancer risk: a meta-analysis. genetics_GWAS hsa-mir-146a Carcinoma, Colon 27824903 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 miR-146a Polymorphism (rs2910164) Predicts Colorectal Cancer Patients' Susceptibility to Liver Metastasis. genetics_GWAS hsa-mir-149 Carcinoma, Colon 27706637 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 MicroRNA variants and colorectal cancer risk: a meta-analysis. genetics_GWAS hsa-mir-196a Carcinoma, Colon 27706637 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 MicroRNA variants and colorectal cancer risk: a meta-analysis. genetics_GWAS hsa-mir-19a Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-19b Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-214 Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-25 Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-27a Carcinoma, Colon 27706637 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 MicroRNA variants and colorectal cancer risk: a meta-analysis. genetics_GWAS hsa-mir-27a Carcinoma, Colon 27751356 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Association between microRNA-27a rs895819 polymorphism and risk of colorectal cancer: A meta-analysis. genetics_GWAS hsa-mir-499 Carcinoma, Colon 27706637 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 MicroRNA variants and colorectal cancer risk: a meta-analysis. genetics_GWAS hsa-mir-525 Carcinoma, Colon 26630397 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Of the 327 SNPs identified in the literature as being important because of their potential regulation of miRNA expression levels, 12.5% had statistically significantly associations with miRNA expression. However, only two of these SNPs were significantly associated with colon cancer. genetics_GWAS hsa-mir-608 Carcinoma, Colon 28653886 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 The miR-608 rs4919510 polymorphism may modify cancer susceptibility based on type. genetics_GWAS hsa-mir-34b Carcinoma, Esophageal 24260422 disease of cellular proliferation DOID:1107 C15.9 D004938 133239 HP:0011459 Hsa-miR-34b/c rs4938723 T>C and hsa-miR-423 rs6505162 C>A polymorphisms are associated with the risk of esophageal cancer in a Chinese population. genetics_GWAS hsa-mir-34c Carcinoma, Esophageal 24260422 disease of cellular proliferation DOID:1107 C15.9 D004938 133239 HP:0011459 Hsa-miR-34b/c rs4938723 T>C and hsa-miR-423 rs6505162 C>A polymorphisms are associated with the risk of esophageal cancer in a Chinese population. genetics_GWAS hsa-mir-423 Carcinoma, Esophageal 24260422 disease of cellular proliferation DOID:1107 C15.9 D004938 133239 HP:0011459 Hsa-miR-34b/c rs4938723 T>C and hsa-miR-423 rs6505162 C>A polymorphisms are associated with the risk of esophageal cancer in a Chinese population. genetics_GWAS hsa-mir-218 Carcinoma, Gastric 28298809 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Predictive Value of MiR-219-1, MiR-938, MiR-34b/c, and MiR-218 Polymorphisms for Gastric Cancer Susceptibility and Prognosis. genetics_GWAS hsa-mir-219 Carcinoma, Gastric 28298809 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Predictive Value of MiR-219-1, MiR-938, MiR-34b/c, and MiR-218 Polymorphisms for Gastric Cancer Susceptibility and Prognosis. genetics_GWAS hsa-mir-27b Carcinoma, Gastric 28214904 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 rs10719 Polymorphism Located within DROSHA 3'-Untranslated Region is Responsible for Development of Primary Hypertension by Disrupting Binding with microRNA-27b. genetics_GWAS hsa-mir-34b Carcinoma, Gastric 28298809 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Predictive Value of MiR-219-1, MiR-938, MiR-34b/c, and MiR-218 Polymorphisms for Gastric Cancer Susceptibility and Prognosis. genetics_GWAS hsa-mir-34c Carcinoma, Gastric 28298809 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Predictive Value of MiR-219-1, MiR-938, MiR-34b/c, and MiR-218 Polymorphisms for Gastric Cancer Susceptibility and Prognosis. genetics_GWAS hsa-mir-526b Carcinoma, Gastric 24595048 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 The has-miR-526b binding-site rs8506G>a polymorphism in the lincRNA-NR_024015 exon identified by GWASs predispose to non-cardia gastric cancer risk. genetics_GWAS hsa-mir-938 Carcinoma, Gastric 28298809 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Predictive Value of MiR-219-1, MiR-938, MiR-34b/c, and MiR-218 Polymorphisms for Gastric Cancer Susceptibility and Prognosis. genetics_GWAS hsa-mir-101 Carcinoma, Hepatocellular 28366737 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miRNA-101-1 and miRNA-221 expressions and their polymorphisms as biomarkers for early diagnosis of hepatocellular carcinoma. genetics_GWAS hsa-mir-101-1 Carcinoma, Hepatocellular 26434859 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our results revealed no significant association between miR-149 (rs2292832) and miR-101-1 (rs7536540) and the risk of HCC in our Thai population.However, this research is the first study of miR-149 (rs2292832) and miR-101-1 (rs7536541) in HCC in Thai populations and the results need to be confirmed with a larger population. genetics_GWAS hsa-mir-106b Carcinoma, Hepatocellular 22393390 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)=0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR=1.25, 95% CIs=1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues. genetics_GWAS hsa-mir-106b Carcinoma, Hepatocellular 24416400 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A genetic variant in the promoter region of miR-106b-25 cluster predict clinical outcome of HBV-related hepatocellular carcinoma in Chinese. genetics_GWAS hsa-mir-122 Carcinoma, Hepatocellular 24995424 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A genetic variant in microRNA-122 regulatory region confers risk for chronic hepatitis B virus infection and hepatocellular carcinoma in Han Chinese. genetics_GWAS hsa-mir-122 Carcinoma, Hepatocellular 28512857 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Interest of variations in microRNA-152 and -122 in a series of hepatocellular carcinomas related to hepatitis C virus infection. genetics_GWAS hsa-mir-1231 Carcinoma, Hepatocellular 22824466 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A miR-1231 binding site polymorphism (rs17875871) in the 3'UTR of IFNAR1 is associated with hepatocellular carcinoma susceptibility. genetics_GWAS hsa-mir-125a Carcinoma, Hepatocellular 27814341 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association Between microRNA-125a rs12976445 C>T Polymorphism and 18F-Fluorodeoxyglucose (18FDG) Uptake: Clinical and Metabolic Response in Patients with Non-Small Cell Lung Cancer. genetics_GWAS hsa-mir-1269a Carcinoma, Hepatocellular 28081866 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A single nucleotide variant in microRNA-1269a promotes the occurrence and process of hepatocellular carcinoma by targeting to oncogenes SPATS2L and LRP6. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 18711148 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-146a: A functional polymorphism (rs2910164) in the miR-146a gene is associated with the risk for hepatocellular carcinoma genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 24377574 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our results demonstrate that miR-196a4 CC genotype and C allele have an important role in HCC risk in Chinese, especially in patients with HBV infection. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 24587132 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 These results suggest that a significant association exists between miRNA499 SNPs and hepatocellular carcinoma. Gene-environment interactions of miRNA499 polymorphisms, smoking, and alcohol consumption might alter hepatocellular carcinoma susceptibility. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 24615520 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-146a G>C polymorphisms and risk of hepatocellular carcinoma in a Chinese population. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 24816919 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association between miR-146aG>C and miR-196a2C>T polymorphisms and the risk of hepatocellular carcinoma in a Chinese population. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 25546664 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 the miR-146a rs2910164 polymorphism contributes to increased HCC susceptibility, especially in Asian populations. Further large and well-designed studies are required to validate this association. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 27706712 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Contributions of polymorphisms in miR146a, miR196a, and miR499 to the development of hepatocellular carcinoma. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 27886162 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-146a rs2910164 and hepatocellular carcinoma: a meta-analysis. genetics_GWAS hsa-mir-146a Carcinoma, Hepatocellular 28188097 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our findings supported the proposition that the polymorphisms of miR-146a rs2910164, miR-196a2 rs11614913, and miR-196a2 rs11614913 may contribute to the susceptibility of HCC genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 24587132 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 These results suggest that a significant association exists between miRNA499 SNPs and hepatocellular carcinoma. Gene-environment interactions of miRNA499 polymorphisms, smoking, and alcohol consumption might alter hepatocellular carcinoma susceptibility. genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 25061729 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association of miR-149C>T and miR-500A>G polymorphisms with the risk of hepatocellular carcinoma in the Chinese population. genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 26434859 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our results revealed no significant association between miR-149 (rs2292832) and miR-101-1 (rs7536540) and the risk of HCC in our Thai population.However, this research is the first study of miR-149 (rs2292832) and miR-101-1 (rs7536540) in HCC in Thai populations and the results need to be confirmed with a larger population. genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 24040059 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Results of this meta-analysis suggest that the hsa-miR-149 rs2292832 polymorphism is not associated with cancer risk in spite of the potentially protective role of C allele in hepatocellular carcinoma and male gastric cancer. genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 26823863 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Predictive role of miR-146a rs2910164 (C>G), miR-149 rs2292832 (T>C), miR-196a2 rs11614913 (T>C) and miR-499 rs3746444 (T>C) in the development of hepatocellular carcinoma. genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 27141902 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A meta-analysis of microRNA-149, microRNA-499 gene polymorphism and susceptibility to hepatocellular carcinoma genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 27348444 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 MIR-149 gene rs2292832 polymorphism contributed to the risk of HCC genetics_GWAS hsa-mir-149 Carcinoma, Hepatocellular 25222224 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Role of miR-149C>T polymorphisms on the risk of hepatocellular carcinoma in a Chinese population. genetics_GWAS hsa-mir-196 Carcinoma, Hepatocellular 24587132 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 These results suggest that a significant association exists between miRNA499 SNPs and hepatocellular carcinoma. Gene-environment interactions of miRNA499 polymorphisms, smoking, and alcohol consumption might alter hepatocellular carcinoma susceptibility. genetics_GWAS hsa-mir-196a Carcinoma, Hepatocellular 24377574 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our results demonstrate that miR-196a2 CC genotype and C allele have an important role in HCC risk in Chinese, especially in patients with HBV infection. genetics_GWAS hsa-mir-196a Carcinoma, Hepatocellular 27706712 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Contributions of polymorphisms in miR146a, miR196a, and miR499 to the development of hepatocellular carcinoma. genetics_GWAS hsa-mir-196a Carcinoma, Hepatocellular 28188097 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our findings supported the proposition that the polymorphisms of miR-146a rs2910164, miR-196a2 rs11614913, and miR-196a2 rs11614913 may contribute to the susceptibility of HCC genetics_GWAS hsa-mir-196a-2 Carcinoma, Hepatocellular 26464719 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 In conclusion, miR-196a2 rs11614913 polymorphism may contribute to identifying individuals, especially in HBV-infected subjects, who are at high risk for HCC. genetics_GWAS hsa-mir-196a-2 Carcinoma, Hepatocellular 20188135 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-196a2:MIR196A2 polymorphism was associated with susceptibility to HBV-related HCC in a maleChinese population. genetics_GWAS hsa-mir-196a-2 Carcinoma, Hepatocellular 23791656 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Three common functional polymorphisms in microRNA encoding genes in the susceptibility to hepatocellular carcinoma: a systematic review and meta-analysis. genetics_GWAS hsa-mir-196a-2 Carcinoma, Hepatocellular 24816919 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association between miR-146aG>C and miR-196a2C>T polymorphisms and the risk of hepatocellular carcinoma in a Chinese population. genetics_GWAS hsa-mir-196a-2 Carcinoma, Hepatocellular 26365437 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 In conclusion,the donor miR-196a-2 rs11614913 polymorphism is associated with HCC recurrence after LT and improves the predictive value of clinical models. The overexpression of miR-196a in the liver might provide a tumor-favorable environment for the development of HCC. genetics_GWAS hsa-mir-196a-2 Carcinoma, Hepatocellular 25546664 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 the miR-146a rs2910165 polymorphism contributes to increased HCC susceptibility, especially in Asian populations. Further large and well-designed studies are required to validate this association. genetics_GWAS hsa-mir-214 Carcinoma, Hepatocellular 27619679 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 U/G SNP rs111904020 in 3'UTR of STAT3 regulated by miR-214 promotes hepatocellular carcinoma development in Chinese population. genetics_GWAS hsa-mir-218 Carcinoma, Hepatocellular 24118778 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 rs11134527 may be a novel genetic risk factor of HCC in HBV-exposed subjects, can facilitate HBV preS deletion generation and predispose the host to the effect of T1674C/G and preS1 start codon mutation in hepatocarcinogenesis. genetics_GWAS hsa-mir-218-1 Carcinoma, Hepatocellular 22011248 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The AG genotype of pri-miR-218 rs11134527 A/G was associated with family history (p=0.018, odds ratio [OR]=2.96, 95% confidence interval [CI]: 1.16-7.56) and elevated serum alpha-fetoprotein (serum alpha-fetoprotein [AFP]) levels (≥20 ng/mL; p=0.009, OR=1.92, 95% CI: 1.17-3.14) in HCC patients. These findings suggested that the AG genotype of pri-miR-218 rs11134527 might relate to genetic predisposition and be involved in regulating the expression of AFP in Chinese HCC patients. genetics_GWAS hsa-mir-218-2 Carcinoma, Hepatocellular 22011248 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The AG genotype of pri-miR-218 rs11134527 A/G was associated with family history (p=0.018, odds ratio [OR]=2.96, 95% confidence interval [CI]: 1.16-7.56) and elevated serum alpha-fetoprotein (serum alpha-fetoprotein [AFP]) levels (≥20 ng/mL; p=0.009, OR=1.92, 95% CI: 1.17-3.14) in HCC patients. These findings suggested that the AG genotype of pri-miR-218 rs11134527 might relate to genetic predisposition and be involved in regulating the expression of AFP in Chinese HCC patients. genetics_GWAS hsa-mir-221 Carcinoma, Hepatocellular 28366737 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miRNA-101-1 and miRNA-221 expressions and their polymorphisms as biomarkers for early diagnosis of hepatocellular carcinoma. genetics_GWAS hsa-mir-25 Carcinoma, Hepatocellular 22393390 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)=0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR=1.25, 95% CIs=1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues. genetics_GWAS hsa-mir-3131 Carcinoma, Hepatocellular 28034876 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 An indel polymorphism within pre-miR3131 confers risk for hepatocellular carcinoma. genetics_GWAS hsa-mir-34a Carcinoma, Hepatocellular 25179842 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 A functional variant at miR-34a binding site in toll-like receptor 4 gene alters susceptibility to hepatocellular carcinoma in a Chinese Han population. genetics_GWAS hsa-mir-34b Carcinoma, Hepatocellular 23935875 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Lack of association of MiR-34b/c polymorphism (rs4938723) with hepatocellular carcinoma: a meta-analysis. genetics_GWAS hsa-mir-34b Carcinoma, Hepatocellular 27808368 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association between polymorphisms in the promoter region of pri-miR-34b/c and risk of hepatocellular carcinoma. genetics_GWAS hsa-mir-34c Carcinoma, Hepatocellular 27808368 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association between polymorphisms in the promoter region of pri-miR-34b/c and risk of hepatocellular carcinoma. genetics_GWAS hsa-mir-378 Carcinoma, Hepatocellular 24751683 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 These findings indicate that rs1076064 may be a biomarker for HCC susceptibility and prognosis through altering pri-miR-378 transcription. genetics_GWAS hsa-mir-492 Carcinoma, Hepatocellular 26753964 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-492G>C polymorphism (rs2289030) is associated with overall survival of hepatocellular carcinoma patients. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 23791656 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Three common functional polymorphisms in microRNA encoding genes in the susceptibility to hepatocellular carcinoma: a systematic review and meta-analysis. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 24301908 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-499A>G rs3746444 and miR-146aG>C expression and hepatocellular carcinoma risk in the Chinese population. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 24377574 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our results demonstrate that miR-196a3 CC genotype and C allele have an important role in HCC risk in Chinese, especially in patients with HBV infection. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 24587132 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 These results suggest that a significant association exists between miRNA499 SNPs and hepatocellular carcinoma. Gene-environment interactions of miRNA499 polymorphisms, smoking, and alcohol consumption might alter hepatocellular carcinoma susceptibility. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 24816919 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association between miR-146aG>C and miR-196a2C>T polymorphisms and the risk of hepatocellular carcinoma in a Chinese population. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 24854593 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-499 rs3746444 may contribute to the risk and prognosis of HCC, indicating that this SNP could be developed as a biomarker for HCC prediction. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 25867338 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 subjects carrying the miR-499 A allele showed a greatly increased risk of HCC in subjects infected with HBV compared with subjects carrying the miR-499 A allele, with an adjusted odds ratio (95% confidence interval) of 1.53 (1.34-2.41). In conclusion, the miR-146aG>C and miR-499A>G polymorphisms do not have a role in the genetic susceptibility to HCC. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 27706712 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Contributions of polymorphisms in miR146a, miR196a, and miR499 to the development of hepatocellular carcinoma. genetics_GWAS hsa-mir-499 Carcinoma, Hepatocellular 27453271 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-499 rs3746444 was significantly associated with an increased the risk of HCC. genetics_GWAS hsa-mir-499a Carcinoma, Hepatocellular 25061729 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Association of miR-149C>T and miR-499A>G polymorphisms with the risk of hepatocellular carcinoma in the Chinese population. genetics_GWAS hsa-mir-501 Carcinoma, Hepatocellular 27310251 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 We identified a novel SNP located in miR-501 acting as an important factor of the HCC susceptibility genetics_GWAS hsa-mir-502 Carcinoma, Hepatocellular 22095217 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 We analysed a single nucleotide polymorphism (rs16917496) within the miR-502 microRNA seed region for the 3' UTR of SET8 in Chinese hepatocellular carcinoma (HCC) patients. The SET8 CC genotype was independently associated with longer post-operative survival in HCC patients by multivariate analysis (relative risk, 0.175; 95% CI, 0.053 - 0.577; p = 0.004). The SET8 CC genotype was associated with reduced SET8 protein levels based on the immunostaining of 51 HCC tissue samples. We also found the low SET8 levels was associated with longer HCC survival. Our data suggest that SET8 modifies HCC outcome by altering its expression, which depends, at least in part, on its binding affinity with miR502. genetics_GWAS hsa-mir-604 Carcinoma, Hepatocellular 25408584 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The T allele at miR-604 rs2368392 may be a risk allele for the chronicity of HBV infection, but may be a protective allele for the progression to HCC in chronic HBV carriers. genetics_GWAS hsa-mir-608 Carcinoma, Hepatocellular 26815502 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 MiR-608 rs4919510 is associated with prognosis of hepatocellular carcinoma. genetics_GWAS hsa-mir-646 Carcinoma, Hepatocellular 25177719 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our findings support the view that the miR-646 SNP rs6513497 may contribute to the susceptibility of HCC. genetics_GWAS hsa-mir-146a Carcinoma, Lung 24246082 disease of cellular proliferation DOID:3905 C34.90 D008175 The rs2910164 C allele in pre-miR-146a and rs11614913 C allele in pre-miR-196a2 were associated with increased genetic damage levels in coke oven workers genetics_GWAS hsa-mir-196a-2 Carcinoma, Lung 24246082 disease of cellular proliferation DOID:3905 C34.90 D008175 The rs2910164 C allele in pre-miR-146a and rs11614913 C allele in pre-miR-196a2 were associated with increased genetic damage levels in coke oven workers genetics_GWAS hsa-mir-429 Carcinoma, Lung, Non-Small-Cell 27374108 C34.90 D002289 HP:0030358 rs9660710 in miR-200b/200a/429 cluster and rs763354 in miR-30a might modify the susceptibility to NSCLC. genetics_GWAS hsa-mir-4293 Carcinoma, Lung, Non-Small-Cell 28410417 C34.90 D002289 HP:0030358 Genetic variant of miR-4293 rs12220909 is associated with susceptibility to non-small cell lung cancer in a Chinese Han population. genetics_GWAS hsa-let-7a Carcinoma, Lung, Non-Small-Cell 18922928 C34.90 D002289 HP:0030358 A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk. genetics_GWAS hsa-let-7a-1 Carcinoma, Lung, Non-Small-Cell 18922928 C34.90 D002289 HP:0030358 A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk. genetics_GWAS hsa-let-7a-2 Carcinoma, Lung, Non-Small-Cell 18922928 C34.90 D002289 HP:0030358 A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk. genetics_GWAS hsa-let-7a-3 Carcinoma, Lung, Non-Small-Cell 18922928 C34.90 D002289 HP:0030358 A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk. genetics_GWAS hsa-let-7b Carcinoma, Lung, Non-Small-Cell 18922928 C34.90 D002289 HP:0030358 A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk. genetics_GWAS hsa-let-7d Carcinoma, Lung, Non-Small-Cell 18922928 C34.90 D002289 HP:0030358 A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk. genetics_GWAS hsa-let-7g Carcinoma, Lung, Non-Small-Cell 18922928 C34.90 D002289 HP:0030358 A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk. genetics_GWAS hsa-mir-146a Carcinoma, Lung, Non-Small-Cell 21902575 C34.90 D002289 HP:0030358 CG genotype of miR-146a(rs2910164 C-G) appeared associated to an increased risk for NSCLC (p=0.042 and 1.77 OR). genetics_GWAS hsa-mir-146b Carcinoma, Lung, Non-Small-Cell 21902575 C34.90 D002289 HP:0030358 CG genotype of miR-146a(rs2910164 C-G) appeared associated to an increased risk for NSCLC (p=0.042 and 1.77 OR). genetics_GWAS hsa-mir-17 Carcinoma, Lung, Non-Small-Cell 25716425 C34.90 D002289 HP:0030358 The rs3660G>C affects KRT81 expression and thus influences survival in early-stage NSCLC. The analysis of the rs3660G>C polymorphism may be useful to identify patients at high risk of a poor disease outcome. genetics_GWAS hsa-mir-196a-2 Carcinoma, Lung, Non-Small-Cell 21617338 C34.90 D002289 HP:0030358 MicroRNA196a2 rs11614913 Genotypes are associated with the Risk of Non-Small Cell Lung Cancer in Korean Population. genetics_GWAS hsa-mir-196a-2 Carcinoma, Lung, Non-Small-Cell 21902575 C34.90 D002289 HP:0030358 The authors clearly detected a significant increase (p<0.001) of miR-196a2 expression in NSCLC. In particular the authors found a significant association between miR-196a2 (rs11614913 C-T) CC genotype and high expression, whereas TT genotype showed a very low expression in comparison to both CT (p<0.005) and CC patients (p<0.01). genetics_GWAS hsa-mir-196a-2 Carcinoma, Lung, Non-Small-Cell 24853117 C34.90 D002289 HP:0030358 Importantly, this method can be further applied to analyze the point mutation of mir-196a2 in the lung tissues of non small-cell lung cancer patients. genetics_GWAS hsa-mir-20b Carcinoma, Lung, Non-Small-Cell 25716425 C34.90 D002289 HP:0030358 The rs3660G>C affects KRT81 expression and thus influences survival in early-stage NSCLC. The analysis of the rs3660G>C polymorphism may be useful to identify patients at high risk of a poor disease outcome. genetics_GWAS hsa-mir-27a Carcinoma, Lung, Non-Small-Cell 24223174 C34.90 D002289 HP:0030358 Our results suggest that the pre-miR-27a rs895819 polymorphism may influence NSCLC patients' clinical outcome. Further large sample studies should be used to validate our findings. genetics_GWAS hsa-mir-502 Carcinoma, Lung, Non-Small-Cell 24146953 C34.90 D002289 HP:0030358 Our data suggested that the rs16917496 T>C located at miR-502 binding site contributes to NSCLC survival by altering SET8 expression through modulating miRNA-target interaction. genetics_GWAS hsa-mir-502 Carcinoma, Lung, Non-Small-Cell 24374662 C34.90 D002289 HP:0030358 Association of miR-502-binding site single nucleotide polymorphism in the 3'-untranslated region of SET8 and TP53 codon 72 polymorphism with non-small cell lung cancer in Chinese population. genetics_GWAS hsa-mir-1827 Carcinoma, Lung, Small-Cell 21676885 C34.90 D055752 182280 HP:0030357 Genetic Variation in an miRNA-1827 Binding Site in MYCL1 Alters Susceptibility to Small-Cell Lung Cancer. The rs3134615T allele was associated with a significantly increased risk of SCLC, with the OR for carrying the GT or TT genotype being 2.08 (95% confidence interval, 1.39-3.21; P = 0.0004) compared with the GG genotype. genetics_GWAS hsa-mir-608 Carcinoma, Nasopharyngeal 23796562 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 A sequence polymorphism in miR-608 predicts recurrence after radiotherapy for nasopharyngeal carcinoma. genetics_GWAS hsa-mir-608 Carcinoma, Nasopharyngeal 25861865 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Polymorphism in mature microRNA-608 sequence is associated with an increased risk of nasopharyngeal carcinoma. genetics_GWAS hsa-mir-1269b Carcinoma, Oral 27525378 gastrointestinal system disease DOID:0050610 Genetic variants in microRNA-146a (C>G) and microRNA-1269b (G>C) are associated with the decreased risk of oral premalignant lesions, oral cancer, and pharyngeal cancer. genetics_GWAS hsa-mir-146a Carcinoma, Oral 27525378 gastrointestinal system disease DOID:0050610 Genetic variants in microRNA-146a (C>G) and microRNA-1269b (G>C) are associated with the decreased risk of oral premalignant lesions, oral cancer, and pharyngeal cancer. genetics_GWAS hsa-mir-101 Carcinoma, Ovarian 21765906 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 a few of which have been found in the genomic fragile regions that are associated with abnormal deletion or amplification in cancer, such as miR-21, miR-101-1, miR-210 and miR-301a. genetics_GWAS hsa-mir-146a Carcinoma, Ovarian 27706635 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 miR-146a and miR-196a2 polymorphisms in ovarian cancer risk. genetics_GWAS hsa-mir-196a2 Carcinoma, Ovarian 27706635 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 miR-146a and miR-196a2 polymorphisms in ovarian cancer risk. genetics_GWAS hsa-mir-21 Carcinoma, Ovarian 21765906 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 a few of which have been found in the genomic fragile regions that are associated with abnormal deletion or amplification in cancer, such as miR-21, miR-101-1, miR-210 and miR-301a. genetics_GWAS hsa-mir-210 Carcinoma, Ovarian 21765906 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 a few of which have been found in the genomic fragile regions that are associated with abnormal deletion or amplification in cancer, such as miR-21, miR-101-1, miR-210 and miR-301a. genetics_GWAS hsa-mir-301a Carcinoma, Ovarian 21765906 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 a few of which have been found in the genomic fragile regions that are associated with abnormal deletion or amplification in cancer, such as miR-21, miR-101-1, miR-210 and miR-301a. genetics_GWAS hsa-mir-34b Carcinoma, Prostate 27983526 disease of cellular proliferation DOID:10286 D07.5 D011471 176807 HP:0012125 Pri-miR-34b/c rs4938723 polymorphism increased the risk of prostate cancer. genetics_GWAS hsa-mir-34c Carcinoma, Prostate 27983526 disease of cellular proliferation DOID:10286 D07.5 D011471 176807 HP:0012125 Pri-miR-34b/c rs4938723 polymorphism increased the risk of prostate cancer. genetics_GWAS hsa-mir-146a Carcinoma, Renal Cell 26323945 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 the observed association between the GG and GC genotype and poorer survival rate of RCC was at least partially mediated by the decreased expression of miR-146a. genetics_GWAS hsa-mir-149 Carcinoma, Renal Cell 24681820 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 We genotyped four common miRNA SNPs (i.e. miR-146a rs2910164, miR-149 rs2292832, miR-196a2 rs11614913 and miR-499 rs3746444) to assess their associations with RCC risk in a two-stage case-control study (355 cases and 362 controls in discovery set, meanwhile 647 cases and 660 controls in validation set), as well as RCC survival in 311 patients. genetics_GWAS hsa-mir-27a Carcinoma, Renal Cell 23118855 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 A genetic variant in pre-miR-27a is associated with a reduced renal cell cancer risk in a Chinese population genetics_GWAS hsa-mir-34b Carcinoma, Renal Cell 24503183 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 A potentially functional polymorphism in the promoter region of miR-34b/c is associated with renal cell cancer risk in a Chinese population. genetics_GWAS hsa-mir-34c Carcinoma, Renal Cell 24503183 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 A potentially functional polymorphism in the promoter region of miR-34b/c is associated with renal cell cancer risk in a Chinese population. genetics_GWAS hsa-mir-502 Carcinoma, Renal Cell, Clear-Cell 27346408 disease of cellular proliferation DOID:4467 HP:0006770 Polymorphism at the miR-502 binding site in the 3' untranslated region of SET8 gene is associated with the risk of clear cell renal cell carcinoma genetics_GWAS hsa-mir-146a Carcinoma, Thyroid, Papillary 26722556 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 Our study indicated that the miR-146a polymorphism was significantly associated with PTC risk. In contrast, meta-analysis revealed no evidence of association between miR-146a variants and PTC risk. Further studies are required to elucidate the role of miR-146a in the etiology of PTC. genetics_GWAS hsa-mir-34b Carcinoma, Thyroid, Papillary 26402809 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 These findings indicate that the miR-34b/c rs4938723 and TP-53 Arg72Pro polymorphisms may contribute to the susceptibility of PTC. genetics_GWAS hsa-mir-34c Carcinoma, Thyroid, Papillary 26402809 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 These findings indicate that the miR-34b/c rs4938723 and TP-53 Arg72Pro polymorphisms may contribute to the susceptibility of PTC. genetics_GWAS hsa-mir-320e Cardiometabolic Disorders 25814643 We provide evidence for a model in which polymorphisms in miRNA-binding sites can both positively and negatively affect miRNA-mediated regulation of cardiometabolic genes. genetics_GWAS hsa-mir-196a-2 Cardiomyopathy, Dilated 20488170 cardiovascular system disease DOID:12930 I42.0 D002311 115200 HP:0001644 mir-196a2:Common genetic polymorphisms in pre-microRNAs were associated with increased risk of dilated cardiomyopathy genetics_GWAS hsa-mir-499a Cardiomyopathy, Dilated 20488170 cardiovascular system disease DOID:12930 I42.0 D002311 115200 HP:0001644 mir-499:Common genetic polymorphisms in pre-microRNAs were associated with increased risk of dilated cardiomyopathy genetics_GWAS hsa-mir-208b Cardiomyopathy, Hypertrophic 25633875 cardiovascular system disease DOID:11984 I42.2 D002312 192600 HP:0001639 Sequence variants in miRNAs of patients with HCM are not frequent and the contribution of these variants to the development of this disease was not demonstrated. genetics_GWAS hsa-mir-367 Cardiomyopathy, Hypertrophic 25633875 cardiovascular system disease DOID:11984 I42.2 D002312 192600 HP:0001639 Sequence variants in miRNAs of patients with HCM are not frequent and the contribution of these variants to the development of this disease was not demonstrated. genetics_GWAS hsa-mir-146a Cardiovascular Diseases [unspecific] 25865299 D002318 Association of miR-146a rs2910164 polymorphism with cardio-cerebrovascular diseases: A systematic review and meta-analysis. genetics_GWAS hsa-mir-146a Carotid Atherosclerosis 26505665 I65.29 D002340 The miR-146a rs2910164 polymorphism might be associated with carotid vulnerable plaque risk in Chinese type 2 diabetes mellitus patients, particularly in older patients, females, those with diabetes duration of more than 10 years and those with hypertension. The transcriptional coactivator p300 rs20551 polymorphism may not be a risk factor for the development or progression of atherosclerosis in type 2 diabetes mellitus. genetics_GWAS hsa-mir-125b Cataract 27431420 nervous system disease DOID:83 H26.9 D002386 PS116200 HP:0000518 rs78378222 polymorphism in the 3'-untranslated region of TP53 contributes to development of age-associated cataracts by modifying microRNA-125b-induced apoptosis of lens epithelial cells. genetics_GWAS hsa-mir-184 Cataract 24138095 nervous system disease DOID:83 H26.9 D002386 PS116200 HP:0000518 C.57 C > T Mutation in MIR 184 is Responsible for Congenital Cataracts and Corneal Abnormalities in a Five-generation Family from Galicia, Spain. genetics_GWAS hsa-mir-149 Charcot-Marie-Tooth Disease Type 1A 29729827 musculoskeletal system disease DOID:0110148 G60.0 D002607 118220 Association of miR-149 polymorphism with onset age and severity in Charcot-Marie-Tooth disease type 1A. genetics_GWAS hsa-mir-196a-2 Chronic Hepatitis B 24248733 B18.0-.1 D019694 610424 MicroRNA-196A-2 polymorphisms and hepatocellular carcinoma in patients with chronic hepatitis B. genetics_GWAS hsa-mir-122 Chronic Hepatitis C 28082397 B18.2 D019698 609532 Differential hepatitis C virus RNA target site selection and host factor activities of naturally occurring miR-122 3΄ variants. genetics_GWAS hsa-mir-146a Chronic Obstructive Pulmonary Disease 25767384 respiratory system disease DOID:3083 J44.9 D029424 606963 HP:0006510 the rs2910164 CC and GC genotype was found to be associated with an improved lung function and milder disease stages, at least partially, mediated by its ability to increase in COX2 expression and PGE2 production. genetics_GWAS hsa-mir-196a-2 Chronic Obstructive Pulmonary Disease 21565178 respiratory system disease DOID:3083 J44.9 D029424 606963 HP:0006510 The TT genotype and T allele of miR-196a2 rs11614913 were significantly associated with a decreased risk for COPD (Chronic obstructive pulmonary disease), compared with the CC genotype and C allele. Similarly, the GG genotype and G allele of miR-499 rs3746444 were associated with a decreased risk for COPD, compared with the AA genotype and A allele. genetics_GWAS hsa-mir-499a Chronic Obstructive Pulmonary Disease 21565178 respiratory system disease DOID:3083 J44.9 D029424 606963 HP:0006510 The TT genotype and T allele of miR-196a2 rs11614913 were significantly associated with a decreased risk for COPD (Chronic obstructive pulmonary disease), compared with the CC genotype and C allele. Similarly, the GG genotype and G allele of miR-499 rs3746444 were associated with a decreased risk for COPD, compared with the AA genotype and A allele. genetics_GWAS hsa-mir-196a Colitis, Ulcerative 28301487 gastrointestinal system disease DOID:8577 K51 D003093 Association of miR-196a-2 and miR-499 variants with ulcerative colitis and their correlation with expression of respective miRNAs. genetics_GWAS hsa-mir-499 Colitis, Ulcerative 28301487 gastrointestinal system disease DOID:8577 K51 D003093 Association of miR-196a-2 and miR-499 variants with ulcerative colitis and their correlation with expression of respective miRNAs. genetics_GWAS hsa-let-7 Colorectal Carcinoma 27234654 disease of cellular proliferation DOID:0080199 C19 D015179 114500 rs868 is associated with lower TGFBR1 expression thereby increasing CRC risk. genetics_GWAS hsa-mir-145 Colorectal Carcinoma 27444415 disease of cellular proliferation DOID:0080199 C19 D015179 114500 These findings indicate that the rs353292 polymorphism is functional and may be a risk factor for the development of CRC. genetics_GWAS hsa-mir-146 Colorectal Carcinoma 23898084 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The current study provides evidence that the miR-146a rs2690164 polymorphism, as the dominant model of the G allele, is associated with the susceptibility and prognosis of CRC. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 24136745 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Association between microRNA genetic variants and susceptibility to colorectal cancer in Chinese population. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 24399071 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Effects of common polymorphisms rs2910164 in miR-146a and rs11614913 in miR-196a2 on susceptibility to colorectal cancer: a systematic review meta-analysis. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 24568449 disease of cellular proliferation DOID:0080199 C19 D015179 114500 These findings supported that the miR-196a2 rs11614913 and miR-149 rs2292832 polymorphisms may contribute to susceptibility to CRC. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 24740563 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Association of a genetic variant in microRNA-146a with risk of colorectal cancer: a population-based case-control study. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 25103961 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Lack of association between miR-27a, miR-146a, miR-196a-2, miR-492 and miR-608 gene polymorphisms and colorectal cancer. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 25283877 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Effect of a common genetic variant microRNA-146a rs2910164 on colorectal cancer: a meta-analysis. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 26813595 disease of cellular proliferation DOID:0080199 C19 D015179 114500 SNPs in the miRNA genes are important for tumorigenesis. The changes by hsa-mir-146a rs1052918 C>G may result in loss of Wnt, constant activation of the Wnt signaling pathway, and uncontrolled cell proliferation and tumor progression. genetics_GWAS hsa-mir-149 Colorectal Carcinoma 24568449 disease of cellular proliferation DOID:0080199 C19 D015179 114500 These findings supported that the miR-196a2 rs11614913 and miR-149 rs2292832 polymorphisms may contribute to susceptibility to CRC. genetics_GWAS hsa-mir-196a Colorectal Carcinoma 24568449 disease of cellular proliferation DOID:0080199 C19 D015179 114500 These findings supported that the miR-196a2 rs11614913 and miR-149 rs2292832 polymorphisms may contribute to susceptibility to CRC. genetics_GWAS hsa-mir-196a-2 Colorectal Carcinoma 24399071 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Effects of common polymorphisms rs2910164 in miR-146a and rs11614913 in miR-196a2 on susceptibility to colorectal cancer: a systematic review meta-analysis. genetics_GWAS hsa-mir-196a-2 Colorectal Carcinoma 25103961 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Lack of association between miR-27a, miR-146a, miR-196a-2, miR-492 and miR-608 gene polymorphisms and colorectal cancer. genetics_GWAS hsa-mir-27a Colorectal Carcinoma 25078482 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Association between miR-27a genetic variants and susceptibility to colorectal cancer. genetics_GWAS hsa-mir-27a Colorectal Carcinoma 25103961 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Lack of association between miR-27a, miR-146a, miR-196a-2, miR-492 and miR-608 gene polymorphisms and colorectal cancer. genetics_GWAS hsa-mir-27a Colorectal Carcinoma 25222241 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Association between a functional variant in microRNA-27a and susceptibility to colorectal cancer in a Chinese Han population. genetics_GWAS hsa-mir-27a Colorectal Carcinoma 25976406 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-27a rs895819 polymorphism was associated with increased risk of colorectal cancer in Chinese population. genetics_GWAS hsa-mir-27a Colorectal Carcinoma 26302683 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Genotype GG of rs895819 Functional Polymorphism Within miR-27a Might Increase Genetic Susceptibility to Colorectal Cancer in Han Chinese Population genetics_GWAS hsa-mir-34b Colorectal Carcinoma 24337371 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Polymorphisms of the pri-miR-34b/c promoter and TP53 codon 72 are associated with risk of colorectal cancer. genetics_GWAS hsa-mir-34b Colorectal Carcinoma 25475831 disease of cellular proliferation DOID:0080199 C19 D015179 114500 rs4938723 was a susceptible locus only for hepatocellular cancer and colorectal cancer. genetics_GWAS hsa-mir-34c Colorectal Carcinoma 24337371 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Polymorphisms of the pri-miR-34b/c promoter and TP53 codon 72 are associated with risk of colorectal cancer. genetics_GWAS hsa-mir-34c Colorectal Carcinoma 25475831 disease of cellular proliferation DOID:0080199 C19 D015179 114500 rs4938723 was a susceptible locus only for hepatocellular cancer and colorectal cancer. genetics_GWAS hsa-mir-3622a Colorectal Carcinoma 26147304 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Our results indicate variations in RAN rs14035, DICER1 rs3742330, XPO5 rs11077, and DROSHA rs10719 of Korean patients are significantly associated with their risk of CRC. genetics_GWAS hsa-mir-370 Colorectal Carcinoma 27354594 disease of cellular proliferation DOID:0080199 C19 D015179 114500 rs2279398G>A may affect the expression of DOK3 by altering the miRNA binding efficiency at the miRNA-binding sites of the 3'-UTR in DOK3, thereby impacting CRC tumorigenesis. genetics_GWAS hsa-mir-423 Colorectal Carcinoma 29419695 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Association of microRNA-423 rs6505162 C>A polymorphism with susceptibility and metastasis of colorectal carcinoma. genetics_GWAS hsa-mir-499 Colorectal Carcinoma 24568449 disease of cellular proliferation DOID:0080199 C19 D015179 114500 These findings supported that the miR-196a2 rs11614913 and miR-149 rs2292832 polymorphisms may contribute to susceptibility to CRC. genetics_GWAS hsa-mir-509 Colorectal Carcinoma 26010608 disease of cellular proliferation DOID:0080199 C19 D015179 114500 These findings suggest that the rs13347C/T in microRNA binding site may be potential biomarkers for genetic susceptibility to CRC. genetics_GWAS hsa-mir-520a Colorectal Carcinoma 25834816 disease of cellular proliferation DOID:0080199 C19 D015179 114500 A functional variant at miR-520a binding site in PIK3CA alters susceptibility to colorectal cancer in a Chinese Han population. genetics_GWAS hsa-mir-5582 Colorectal Carcinoma 26147304 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Our results indicate variations in RAN rs14035, DICER1 rs3742330, XPO5 rs11077, and DROSHA rs10719 of Korean patients are significantly associated with their risk of CRC. genetics_GWAS hsa-mir-603 Colorectal Carcinoma 24934365 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Our data suggest that hsa-miR-603 may be involved in colorectal tumorigenesis, and the genetic polymorphism in hsa-miR-603 is associated with CRC susceptibility. genetics_GWAS hsa-let-7 Colorectal Carcinoma 24890702 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Let-7 microRNA-binding-site polymorphism in the 3'UTR of KRAS and colorectal cancer outcome: a systematic review and meta-analysis. genetics_GWAS hsa-mir-1273c Colorectal Carcinoma 22348132 disease of cellular proliferation DOID:0080199 C19 D015179 114500 hsa-mir-1273c, hsa-mir-1303 and hsa-mir-567, with frequent and sometimes bi-allelic mutations in MSI tumors. genetics_GWAS hsa-mir-1303 Colorectal Carcinoma 22348132 disease of cellular proliferation DOID:0080199 C19 D015179 114500 hsa-mir-1273c, hsa-mir-1303 and hsa-mir-567, with frequent and sometimes bi-allelic mutations in MSI tumors. genetics_GWAS hsa-mir-146a Colorectal Carcinoma 23306950 disease of cellular proliferation DOID:0080199 C19 D015179 114500 A genetic variant in miR-146a modifies colorectal cancer susceptibility in a chinese population genetics_GWAS hsa-mir-196a-2 Colorectal Carcinoma 21241442 disease of cellular proliferation DOID:0080199 C19 D015179 114500 A variant ( rs11614913 ) in microRNA-196a2 is not associated with susceptibility to and progression of colorectal cancer in Chinese. genetics_GWAS hsa-mir-196a-2 Colorectal Carcinoma 21565628 disease of cellular proliferation DOID:0080199 C19 D015179 114500 A Functional Variant in MicroRNA-196a2 (rs11614913 SNP) Is Associated with Susceptibility of Colorectal Cancer in a Chinese Population. genetics_GWAS hsa-mir-196a-2 Colorectal Carcinoma 21815818 disease of cellular proliferation DOID:0080199 C19 D015179 114500 A Functional Polymorphism (rs11614913 (T>C)) in miRNA-196a2 Is Associated with Colorectal Cancer Risk in a Chinese Population. genetics_GWAS hsa-mir-196a-2 Colorectal Carcinoma 22161766 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The authors found a significantly increased colorectal cancer risk with the miR-196a2CC (rs11614913) genotype compared with the TT/CT genotype (AOR=1.50; 95% CI=1.11-2.04; P=0.01; FDR-P=0.04) in Korean population. genetics_GWAS hsa-mir-219-1 Colorectal Carcinoma 22661538 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The mir219-1:rs213210 showed consistent association with death in the training set, the replication set, and combined data set genetics_GWAS hsa-mir-367 Colorectal Carcinoma 23393343 disease of cellular proliferation DOID:0080199 C19 D015179 114500 the functional variant (rs1044129) in the miR-367 binding site of RYR3 may be a potential marker for prognosis in patients following curative surgery for CRC genetics_GWAS hsa-mir-423 Colorectal Carcinoma 22028396 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Two SNPs were identified to be significantly associated with recurrence-free survival and overall survival of the patients. The most significant SNP was rs6505162 in pre-miR-423. Compared to the homozygous wild-type genotype, the variant-containing genotypes of this SNP were significantly associated with both the overall survival (HR=2.12, 95% CI1.34--3.34, P=0.001) and the recurrence-free survival (HR=1.59, 95% CI1.08--2.36, P=0.019). Another SNP, rs4919510 in pre-miR-608, was also associated with altered recurrence-free survival (HR=0.61, 95% CI 0.41-0.92, P=0.017). These effects were evident only in patients receiving chemotherapy but not in those without chemotherapy. In addition, the combined analysis of the two SNPs conferred a 2.84-fold (95% CI 1.50-5.37, P=0.001) increased risk of recurrence and/or death. Similarly, this effect was only prominent in those receiving chemotherapy (P<0.001) but not in those without chemotherapy (P=0.999). genetics_GWAS hsa-mir-483 Colorectal Carcinoma 26235181 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Both the single nucleotide polymorphism variants showed a positive association toward risk of lung cancer. genetics_GWAS hsa-mir-491 Colorectal Carcinoma 21128281 disease of cellular proliferation DOID:0080199 C19 D015179 114500 deleted genetics_GWAS hsa-mir-492 Colorectal Carcinoma 20044760 disease of cellular proliferation DOID:0080199 C19 D015179 114500 mir-492:In a univariate analysis, the progression-free survival of the patients with the combined mir492 C/G and G/G genotype was significantly worse than that of the patients with the mir492 C/C genotype (rs2289030) (P value = 0.0426) genetics_GWAS hsa-mir-520a Colorectal Carcinoma 22553375 disease of cellular proliferation DOID:0080199 C19 D015179 114500 A 3' untranslated region (UTR) mutation was also shown to be associated with increased sensitivity to saracatinib and have a reduced affinity for miR-520a and miR-525a. genetics_GWAS hsa-mir-542 Colorectal Carcinoma 21822307 disease of cellular proliferation DOID:0080199 C19 D015179 114500 A common single-nucleotide polymorphism (T8473CA) in cyclooxygenase-2 disrupts microRNA (miR-542-3p)-mediated regulation. genetics_GWAS hsa-mir-551a Colorectal Carcinoma 26235181 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Both the single nucleotide polymorphism variants showed a positive association toward risk of lung cancer. genetics_GWAS hsa-mir-567 Colorectal Carcinoma 22348132 disease of cellular proliferation DOID:0080199 C19 D015179 114500 hsa-mir-1273c, hsa-mir-1303 and hsa-mir-567, with frequent and sometimes bi-allelic mutations in MSI tumors. genetics_GWAS hsa-mir-608 Colorectal Carcinoma 22028396 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Two SNPs were identified to be significantly associated with recurrence-free survival and overall survival of the patients. The most significant SNP was rs6505162 in pre-miR-423. Compared to the homozygous wild-type genotype, the variant-containing genotypes of this SNP were significantly associated with both the overall survival (HR=2.12, 95% CI1.34--3.34, P=0.001) and the recurrence-free survival (HR=1.59, 95% CI1.08--2.36, P=0.019). Another SNP, rs4919510 in pre-miR-608, was also associated with altered recurrence-free survival (HR=0.61, 95% CI 0.41-0.92, P=0.017). These effects were evident only in patients receiving chemotherapy but not in those without chemotherapy. In addition, the combined analysis of the two SNPs conferred a 2.84-fold (95% CI 1.50-5.37, P=0.001) increased risk of recurrence and/or death. Similarly, this effect was only prominent in those receiving chemotherapy (P<0.001) but not in those without chemotherapy (P=0.999). genetics_GWAS hsa-mir-608 Colorectal Carcinoma 22606253 disease of cellular proliferation DOID:0080199 C19 D015179 114500 rs4919510 in hsa-mir-608 is associated with outcome but not risk of colorectal cancer. genetics_GWAS hsa-mir-608 Colorectal Carcinoma 22661538 disease of cellular proliferation DOID:0080199 C19 D015179 114500 In patients with stage III disease, mir608: rs4919510 was associated with increased risk for both recurrence and death. genetics_GWAS hsa-mir-646 Colorectal Carcinoma 21128281 disease of cellular proliferation DOID:0080199 C19 D015179 114500 deleted genetics_GWAS hsa-mir-143 Congenital Heart Diseases 24752771 cardiovascular system disease DOID:1682 Q24 D006330 617912 HP:0030680 No association of pri-miR-143 rs41291957 polymorphism with the risk of congenital heart disease in a Chinese population. genetics_GWAS hsa-mir-196a2 Congenital Heart Diseases 27813602 cardiovascular system disease DOID:1682 Q24 D006330 617912 HP:0030680 Association of miR-196a2, miR-27a, and miR-499 polymorphisms with isolated congenital heart disease in a Chinese population. genetics_GWAS hsa-mir-27a Congenital Heart Diseases 27813602 cardiovascular system disease DOID:1682 Q24 D006330 617912 HP:0030680 Association of miR-196a2, miR-27a, and miR-499 polymorphisms with isolated congenital heart disease in a Chinese population. genetics_GWAS hsa-mir-499 Congenital Heart Diseases 27813602 cardiovascular system disease DOID:1682 Q24 D006330 617912 HP:0030680 Association of miR-196a2, miR-27a, and miR-499 polymorphisms with isolated congenital heart disease in a Chinese population. genetics_GWAS hsa-mir-1 Coronary Artery Disease 25197382 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 Polymorphism in miRNA-1 target site and circulating miRNA-1 phenotype are associated with the decreased risk and prognosis of coronary artery disease. genetics_GWAS hsa-mir-146 Coronary Artery Disease 24447667 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 A common variant in pre-miR-146 is associated with coronary artery disease risk and its mature miRNA expression. genetics_GWAS hsa-mir-146a Coronary Artery Disease 23794009 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 miR-146a polymorphism influences levels of miR-146a, IRAK-1, and TRAF-6 in young patients with coronary artery disease. genetics_GWAS hsa-mir-146a Coronary Artery Disease 26909569 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 Our data provide the first evidence for the association of miR-146a rs2910164 and TCF21 rs12190287 with CAD in an Iranian population, encouraging further research to elucidate the disease-related effects of miR-146a rs2910164. genetics_GWAS hsa-mir-146a Coronary Artery Disease 27430349 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 miRNA polymorphisms (miR鈥?46a, miR鈥?49, miR鈥?96a2 and miR鈥?99) are associated with the risk of coronary artery disease. genetics_GWAS hsa-mir-149 Coronary Artery Disease 27430349 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 miRNA polymorphisms (miR鈥?46a, miR鈥?49, miR鈥?96a2 and miR鈥?99) are associated with the risk of coronary artery disease. genetics_GWAS hsa-mir-196a2 Coronary Artery Disease 27430349 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 miRNA polymorphisms (miR鈥?46a, miR鈥?49, miR鈥?96a2 and miR鈥?99) are associated with the risk of coronary artery disease. genetics_GWAS hsa-mir-196a-2 Coronary Artery Disease 22159951 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 The variant genotypes CC/CT of hsa-mir-196a2 rs11614913 T → C were not associated with a significantly increased risk of CAD (adjusted OR = 1.02, 95% CI = 0.76-1.38), compared with wide genotype TT, but CC and CC/CT genotypes were associated with 34 and 35% increased risks of serious prognosis of CAD (adjusted HR = 1.34, 95% CI = 1.02-1.75 for CC; adjusted HR = 1.35, 95% CI = 1.03-1.75 for CC/CT). In the variant of hsa-mir-499 rs3746444A → G, GG was associated with the 223% increased risk of CAD (adjusted OR = 3.23, 95% CI = 1.56-6.67). Cox regression analysis showed that age, smoking status, numbers of pathological changes in coronary arteries, rs11614913 T → C, and diabetes mellitus were associated with serious prognosis of CAD. genetics_GWAS hsa-mir-224 Coronary Artery Disease 24676100 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 Coronary heart disease-associated variation in TCF21 disrupts a miR-224 binding site and miRNA-mediated regulation. genetics_GWAS hsa-mir-320b Coronary Artery Disease 25573129 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 The common SNP (rs10916581) in the promoter region of pre-miR-320b-2 might have little contribution to the CHD predisposition in Chinese Han population, and it might not affect circulating miR-320b level. Conventional CHD risk factors (BMI, TC/HDL-C, hypertension and diabetes) might have effects on its circulating level. genetics_GWAS hsa-mir-4513 Coronary Artery Disease 25256095 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 A genetic variant in the seed region of miR-4513 shows pleiotropic effects on lipid and glucose homeostasis, blood pressure, and coronary artery disease. genetics_GWAS hsa-mir-499 Coronary Artery Disease 27430349 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 miRNA polymorphisms (miR鈥?46a, miR鈥?49, miR鈥?96a2 and miR鈥?99) are associated with the risk of coronary artery disease. genetics_GWAS hsa-mir-499a Coronary Artery Disease 22159951 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 The variant genotypes CC/CT of hsa-mir-196a2 rs11614913 T → C were not associated with a significantly increased risk of CAD (adjusted OR = 1.02, 95% CI = 0.76-1.38), compared with wide genotype TT, but CC and CC/CT genotypes were associated with 34 and 35% increased risks of serious prognosis of CAD (adjusted HR = 1.34, 95% CI = 1.02-1.75 for CC; adjusted HR = 1.35, 95% CI = 1.03-1.75 for CC/CT). In the variant of hsa-mir-499 rs3746444A → G, GG was associated with the 223% increased risk of CAD (adjusted OR = 3.23, 95% CI = 1.56-6.67). Cox regression analysis showed that age, smoking status, numbers of pathological changes in coronary arteries, rs11614913 T → C, and diabetes mellitus were associated with serious prognosis of CAD. genetics_GWAS hsa-mir-146a Coronary Restenosis 25053223 cardiovascular system disease DOID:4247 D023903 HP:0004761 we found a negative association for the G/C (P = 0.007) and a positive association for the C/C genotype with the risk of restenosis genetics_GWAS hsa-mir-146a Creutzfeldt-Jakob Disease 29216791 nervous system disease DOID:11949 A81.0 D007562 123400 The associations of two SNPs in miRNA-146a and one SNP in ZBTB38-RASA2 with the disease susceptibility and the clinical features of the Chinese patients of sCJD and FFI. genetics_GWAS hsa-let-7e Crohn Disease 22262659 gastrointestinal system disease DOID:8778 K50 D003424 266600 HP:0100280 The rs10889677 variant in the 3'-untranslated region of the IL-23R gene displays enhanced levels of both mRNA and protein production of IL-23R. This can be attributed to a loss of binding capacity for the microRNAs (miRNAs) Let-7e and Let-7f by the variant allele. genetics_GWAS hsa-let-7f-1 Crohn Disease 22262659 gastrointestinal system disease DOID:8778 K50 D003424 266600 HP:0100280 The rs10889677 variant in the 3'-untranslated region of the IL-23R gene displays enhanced levels of both mRNA and protein production of IL-23R. This can be attributed to a loss of binding capacity for the microRNAs (miRNAs) Let-7e and Let-7f by the variant allele. genetics_GWAS hsa-let-7f-2 Crohn Disease 22262659 gastrointestinal system disease DOID:8778 K50 D003424 266600 HP:0100280 The rs10889677 variant in the 3'-untranslated region of the IL-23R gene displays enhanced levels of both mRNA and protein production of IL-23R. This can be attributed to a loss of binding capacity for the microRNAs (miRNAs) Let-7e and Let-7f by the variant allele. genetics_GWAS hsa-mir-196a Crohn Disease 29152405 gastrointestinal system disease DOID:8778 K50 D003424 266600 HP:0100280 Association of miR-146 rs2910164, miR-196a rs11614913, miR-221 rs113054794 and miR-224 rs188519172 polymorphisms with anti-TNF treatment response in a Greek population with Crohn's disease genetics_GWAS hsa-mir-196a-1 Crohn Disease 21278745 gastrointestinal system disease DOID:8778 K50 D003424 266600 HP:0100280 The common exonic synonymous SNP (c.313C>T) in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn's disease. genetics_GWAS hsa-mir-196a-2 Crohn Disease 21278745 gastrointestinal system disease DOID:8778 K50 D003424 266600 HP:0100280 The common exonic synonymous SNP (c.313C>T) in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn's disease. genetics_GWAS hsa-mir-196b Crohn Disease 21278745 gastrointestinal system disease DOID:8778 K50 D003424 266600 HP:0100280 The common exonic synonymous SNP (c.313C>T) in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn's disease. genetics_GWAS hsa-mir-659 Dementia 18723524 disease of mental health DOID:1307 F03 D003704 127750 HP:0000726 miR-659: Common variation in the miR-659 binding-site of GRN is a major risk factor for TDP43-positive frontotemporal dementia genetics_GWAS hsa-mir-146a Dermatomyositis 24716199 integumentary system disease DOID:10223 M33 D003882 MIRSNP rs2910164 of miR-146a is associated with the muscle involvement in polymyositis/dermatomyositis. genetics_GWAS hsa-mir-214 Diabetes Mellitus 26329304 disease of metabolism DOID:9351 E10-E14 D003920 222100 HP:0000819 We have detected the interactions of hsa-miR-214-5p/hsa-miR-550a-5p and the 3'UTR SNP of the HNF1B gene by in vitro luciferase reporter assays, and propose that the binding of such miRNAs regulates the expression of the HNF1B gene and the susceptibility of T2DM. genetics_GWAS hsa-mir-550a Diabetes Mellitus 26329304 disease of metabolism DOID:9351 E10-E14 D003920 222100 HP:0000819 We have detected the interactions of hsa-miR-214-5p/hsa-miR-550a-5p and the 3'UTR SNP of the HNF1B gene by in vitro luciferase reporter assays, and propose that the binding of such miRNAs regulates the expression of the HNF1B gene and the susceptibility of T2DM. genetics_GWAS hsa-mir-124a Diabetes Mellitus, Type 2 25673459 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Affection of single-nucleotide polymorphisms in miR-27a, miR-124a, and miR-146a on susceptibility to type 2 diabetes mellitus in Chinese Han people. genetics_GWAS hsa-mir-146a Diabetes Mellitus, Type 2 25673459 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Affection of single-nucleotide polymorphisms in miR-27a, miR-124a, and miR-146a on susceptibility to type 2 diabetes mellitus in Chinese Han people. genetics_GWAS hsa-mir-146a Diabetes Mellitus, Type 2 28101643 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Polymorphisms in genes encoding miR-155 and miR-146a are associated with protection to type 1 diabetes mellitus. genetics_GWAS hsa-mir-155 Diabetes Mellitus, Type 2 28101643 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Polymorphisms in genes encoding miR-155 and miR-146a are associated with protection to type 1 diabetes mellitus. genetics_GWAS hsa-mir-196a-2 Diabetes Mellitus, Type 2 24972764 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Our findings suggest that miRNA-196a2 T/C polymorphism (rs11614913) is associated with an increased risk of CVD in type 2 diabetes patients. This provides further insights on pathogenesis of cardiovascular disease in type 2 diabetes patients. genetics_GWAS hsa-mir-27a Diabetes Mellitus, Type 2 25673459 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Affection of single-nucleotide polymorphisms in miR-27a, miR-124a, and miR-146a on susceptibility to type 2 diabetes mellitus in Chinese Han people. genetics_GWAS hsa-mir-27a Diabetes Mellitus, Type 2 27300034 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 The pre-mir-27a variant rs895819 may contribute to type 2 diabetes mellitus susceptibility genetics_GWAS hsa-mir-125 Diabetic Nephropathy 26563755 E10-11.21 D003928 We identified miR-125a as a direct regulator of IL-6R, and the genotype of rs12976445 might be a novel predictor of the development of DN in DM. genetics_GWAS hsa-mir-146a Diabetic Nephropathy 26997512 E10-11.21 D003928 Rs2910164 is significantly associated with microvascular complications DN in patients with T1DM and DME in patients with T2DM. genetics_GWAS hsa-mir-146a Diabetic Retinopathy 26997512 nervous system disease DOID:8947 E10-11.31 D003930 Rs2910164 is significantly associated with microvascular complications DN in patients with T1DM and DME in patients with T2DM. genetics_GWAS hsa-mir-146a Digestive System Neoplasms 25555557 D49.0 D004067 digestive tract neoplasms might associate with miR-146a variants, but not miR-196a2 variants genetics_GWAS hsa-mir-146a Digestive System Neoplasms 24247819 D49.0 D004067 miR-146a gene polymorphism rs2910164 and the risk of digestive tumors: A meta-analysis of 21 case-control studies. genetics_GWAS hsa-mir-196a Digestive System Neoplasms 25555557 D49.0 D004067 digestive tract neoplasms might associate with miR-146a variants, but not miR-196a2 variants genetics_GWAS hsa-mir-34b Digestive System Neoplasms 26320502 D49.0 D004067 The current evidence supports the conclusion that the miR-34b/c rs4938723 polymorphism decreases an individual's susceptibility to digestive cancers. genetics_GWAS hsa-mir-325 Dyspepsia 22438098 gastrointestinal system disease DOID:2321 K30 D004415 Genetic polymorphism ( rs5981521 (C>T)) of pri-microRNA 325, targeting SLC6A4 3'-UTR, is closely associated with the risk of functional dyspepsia in Japan. genetics_GWAS hsa-mir-146a Endometrial Neoplasms 26008204 reproductive system disease DOID:1380 C54.1 D016889 608089 Association of SNPs in miR-146a, miR-196a2, and miR-499 with the risk of endometrial/ovarian cancer. genetics_GWAS hsa-mir-196a-2 Endometrial Neoplasms 26008204 reproductive system disease DOID:1380 C54.1 D016889 608089 Association of SNPs in miR-146a, miR-196a2, and miR-499 with the risk of endometrial/ovarian cancer. genetics_GWAS hsa-mir-200b Endometrial Neoplasms 22194984 reproductive system disease DOID:1380 C54.1 D016889 608089 Luciferase assays and Western blot analysis demonstrated that the miR-200b/200c/429 family recognized the MRE in the 3' UTR of AP-2alpha gene and negatively regulated the expression of endogenous AP-2alpha proteins. SNP rs1045385 A>C variation enhanced AP-2alpha. genetics_GWAS hsa-mir-200c Endometrial Neoplasms 22194984 reproductive system disease DOID:1380 C54.1 D016889 608089 Luciferase assays and Western blot analysis demonstrated that the miR-200b/200c/429 family recognized the MRE in the 3' UTR of AP-2 alpha gene and negatively regulated the expression of endogenous AP-2 alpha proteins. SNP rs1045385 A>C variation enhanced AP-2 alpha expression. genetics_GWAS hsa-mir-429 Endometrial Neoplasms 22194984 reproductive system disease DOID:1380 C54.1 D016889 608089 Luciferase assays and Western blot analysis demonstrated that the miR-200b/200c/429 family recognized the MRE in the 3' UTR of AP-2 alpha gene and negatively regulated the expression of endogenous AP-2 alpha proteins. SNP rs1045385 A>C variation enhanced AP-2 alpha expression. genetics_GWAS hsa-mir-499 Endometrial Neoplasms 26008204 reproductive system disease DOID:1380 C54.1 D016889 608089 Association of SNPs in miR-146a, miR-196a2, and miR-499 with the risk of endometrial/ovarian cancer. genetics_GWAS hsa-let-7a-1 Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7a-2 Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7a-3 Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7b Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7c Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7d Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7e Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7f-1 Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7f-2 Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7g Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-let-7i Endometriosis 22307873 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 The authors detected a KRAS variant allele in 31% of women with endometriosis as opposed to 5% of a large diverse control population. genetics_GWAS hsa-mir-125b Endometriosis 24339876 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 Genetic variation at the miR-125b binding site may play functional roles to protect against endometriosis progression. genetics_GWAS hsa-mir-126 Endometriosis 28277133 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 mir-126 rs4636297 and TGFβRI rs334348 functional gene variants are associated with susceptibility to endometriosis and its severity. genetics_GWAS hsa-mir-520a Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-520b Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-520c Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-520d Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-520e Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-520f Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-520g Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-520h Endometriosis 23364396 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women genetics_GWAS hsa-mir-146a Epilepsy 25891929 nervous system disease DOID:1826 G40 D004827 PS601068 HP:0001250 Our data indicate that the rs57095329 polymorphism in the promoter region of miR-146a is involved in the genetic susceptibility to DRE and the seizures frequency. genetics_GWAS hsa-mir-155 Epilepsy 26425555 nervous system disease DOID:1826 G40 D004827 PS601068 HP:0001250 This study first demonstrates the association of MIR155HG/miR-155 tag SNPs with epilepsy and shows that rare CNVs were found exclusively in epileptic patients, clarifying the genetic role of miR-155 in epilepsy. genetics_GWAS hsa-mir-146a Esophageal Neoplasms 21319225 C15.9 D004938 133239 HP:0100751 SNP (rs2910164 G/C): Significantly increased CSCC risks were found to be associated with G allele of rs2910164 genetics_GWAS hsa-mir-196a-1 Esophageal Neoplasms 22859270 C15.9 D004938 133239 HP:0100751 MiR-196a binding-site SNP (rs6573) regulates RAP1A expression contributing to esophageal squamous cell carcinoma risk and metastasis. genetics_GWAS hsa-mir-196a-2 Esophageal Neoplasms 22859270 C15.9 D004938 133239 HP:0100751 MiR-196a binding-site SNP (rs6573) regulates RAP1A expression contributing to esophageal squamous cell carcinoma risk and metastasis. genetics_GWAS hsa-mir-499a Esophageal Neoplasms 21319225 C15.9 D004938 133239 HP:0100751 SNP (rs3746444 A/G): Significantly increased CSCC risks were found to be associated with G allele of rs3746444 genetics_GWAS hsa-let-7c Essential Hypertension 26274321 cardiovascular system disease DOID:10825 I10 C562386 145500 In conclusion, our experimental results provide evidence that the T allele of rs17168525 in the 3'-UTR of myotrophin might influence the level of myotrophin protein by interfering with let-7/miR-98 binding. genetics_GWAS hsa-mir-503 Essential Hypertension 26274321 cardiovascular system disease DOID:10825 I10 C562386 145500 In conclusion, our experimental results provide evidence that the T allele of rs17168525 in the 3'-UTR of myotrophin might influence the level of myotrophin protein by interfering with let-7/miR-98 binding. genetics_GWAS hsa-mir-98 Essential Hypertension 26274321 cardiovascular system disease DOID:10825 I10 C562386 145500 In conclusion, our experimental results provide evidence that the T allele of rs17168525 in the 3'-UTR of myotrophin might influence the level of myotrophin protein by interfering with let-7/miR-98 binding. genetics_GWAS hsa-let-7a Gastric Neoplasms 24760009 disease of cellular proliferation DOID:10534 C16 D013274 137215 pri-let-7a-2 rs629367 CC genotype could increase the risks of gastric cancer as well as atrophic gastritis and was also associated with poor survival of gastric cancer, which possibly by affecting the mature let-7a expression, and could serve as a predicting biomarker for high-risk and poor prognosis of gastric cancer. genetics_GWAS hsa-mir-125a Gastric Neoplasms 25109760 disease of cellular proliferation DOID:10534 C16 D013274 137215 In this study, we found that a germline mutation in the miR-125a coding region is associated with human gastric cancer. genetics_GWAS hsa-mir-132 Gastric Neoplasms 24981235 disease of cellular proliferation DOID:10534 C16 D013274 137215 A functional variant at miR-132-3p, miR-212-3p, and miR-361-5p binding site in CD80 gene alters susceptibility to gastric cancer in a Chinese Han population. genetics_GWAS hsa-mir-146a Gastric Neoplasms 24379078 disease of cellular proliferation DOID:10534 C16 D013274 137215 Association of the miR-146aC>G, miR-149T>C, and miR-196a2T>C polymorphisms with gastric cancer risk and survival in the Greek population. genetics_GWAS hsa-mir-146a Gastric Neoplasms 24528016 disease of cellular proliferation DOID:10534 C16 D013274 137215 A genetic variant in MiR-146a modifies digestive system cancer risk: a meta-analysis. genetics_GWAS hsa-mir-146a Gastric Neoplasms 25326754 disease of cellular proliferation DOID:10534 C16 D013274 137215 The present meta-analysis suggests an increased risk between miR-146a rs2910164 GG genotype and gastric cancer susceptibility in Chinese based on published literatures. genetics_GWAS hsa-mir-146a Gastric Neoplasms 25386093 disease of cellular proliferation DOID:10534 C16 D013274 137215 The miR-146a rs2910164 polymorphism is associated with increased gastric cancer risk, particularly evident in high quality studies with small sample sized Caucasian populations. genetics_GWAS hsa-mir-146a Gastric Neoplasms 25455160 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-146a rs2910164 polymorphism was associated with the susceptibility to gastric cancer, especially in Asian population. genetics_GWAS hsa-mir-146a Gastric Neoplasms 25795117 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-27a rs895819 and miR-149 rs2292832 are of potential forewarning ability for gastric cancer risk. genetics_GWAS hsa-mir-146a Gastric Neoplasms 26345764 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overall, this meta-analysis failed to detect an association between five common miR-146a gene polymorphisms and GC susceptibility. However, this does not necessarily completely rule out a correlation between miRNA polymorphisms and GC susceptibility. genetics_GWAS hsa-mir-146a Gastric Neoplasms 26345790 disease of cellular proliferation DOID:10534 C16 D013274 137215 In summary, the results suggested that the miR-146a rs2910164 polymorphism was related to gastric cancer risk in Asians but not in Caucasians, and no distinct correlation seemed to exist between the miR-196a-2 rs11614913 polymorphism and the risk of gastric cancer. genetics_GWAS hsa-mir-146a Gastric Neoplasms 23975664 disease of cellular proliferation DOID:10534 C16 D013274 137215 Prognostic role of microRNA polymorphisms in advanced gastric cancer: a translational study of the Arbeitsgemeinschaft Internistische Onkologie (AIO). genetics_GWAS hsa-mir-146a Gastric Neoplasms 21632853 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-146a levels in cancer tissues were significantly lower than those in the corresponding noncancerous tissue. Lower levels of miR-146a were associated with lymph node metastasis and venous invasion. Moreover, a lower level of miR-146a was an independent prognostic factor for overall survival.Ectopic expression of miR-146a inhibited migration and invasion and downregulated EGFR and IRAK1 expression in gastric cancer cells. In addition, G/C SNP within the pre-miR-146a seed sequence significantly reduced miR-146a levels in the GG genotype compared with the CC genotype. genetics_GWAS hsa-mir-146a Gastric Neoplasms 22455393 disease of cellular proliferation DOID:10534 C16 D013274 137215 A Functional Polymorphism (rs2910164) in Pre-miR-146a Is Associated with Susceptibility to Gastric Cancer in a Chinese Population. genetics_GWAS hsa-mir-146a Gastric Neoplasms 27267319 disease of cellular proliferation DOID:10534 C16 D013274 137215 rs2910164 of miR-146a is associated with GC genetics_GWAS hsa-mir-148a Gastric Neoplasms 25399950 disease of cellular proliferation DOID:10534 C16 D013274 137215 the SCRN1 rs6976789 polymorphism may play an important role in the GC development and progression. genetics_GWAS hsa-mir-149 Gastric Neoplasms 24379078 disease of cellular proliferation DOID:10534 C16 D013274 137215 Association of the miR-146aC>G, miR-149T>C, and miR-196a2T>C polymorphisms with gastric cancer risk and survival in the Greek population. genetics_GWAS hsa-mir-149 Gastric Neoplasms 25795117 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-27a rs895819 and miR-149 rs2292832 are of potential forewarning ability for gastric cancer risk. genetics_GWAS hsa-mir-149 Gastric Neoplasms 21976437 disease of cellular proliferation DOID:10534 C16 D013274 137215 Marginally significant associations were found both for hsa-miR-149 rs2292832 with gastric cancer risk (TC+CC vs. TT, OR=0.68, 95% CI: 0.44-1.04) and for hsa-miR-605 rs2043556 with colorectal cancer risk (AG+GG vs. AA, OR=0.70, 95% CI: 0.48-1.02) in males. genetics_GWAS hsa-mir-149 Gastric Neoplasms 26345764 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overall, this meta-analysis failed to detect an association between five common miR-146a gene polymorphisms and GC susceptibility. However, this does not necessarily completely rule out a correlation between miRNA polymorphisms and GC susceptibility. genetics_GWAS hsa-mir-149 Gastric Neoplasms 28523307 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-149 rs2292832 C>T polymorphism and risk of gastric cancer. genetics_GWAS hsa-mir-184 Gastric Neoplasms 23724109 disease of cellular proliferation DOID:10534 C16 D013274 137215 The miR-184 Binding-Site rs8126 T>C Polymorphism in TNFAIP2 Is Associated with Risk of Gastric Cancer. genetics_GWAS hsa-mir-196a-2 Gastric Neoplasms 24379078 disease of cellular proliferation DOID:10534 C16 D013274 137215 Association of the miR-146aC>G, miR-149T>C, and miR-196a2T>C polymorphisms with gastric cancer risk and survival in the Greek population. genetics_GWAS hsa-mir-196a-2 Gastric Neoplasms 25795117 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-27a rs895819 and miR-149 rs2292832 are of potential forewarning ability for gastric cancer risk. genetics_GWAS hsa-mir-196a-2 Gastric Neoplasms 26406571 disease of cellular proliferation DOID:10534 C16 D013274 137215 Our studies suggested that the miR-146a rs2910164 polymorphism might marginally contribute to a decreased risk of gastric cancer, especially in Caucasians, whereas the miR-196a2 rs11614913 polymorphism might not be associated with susceptibility to GC. genetics_GWAS hsa-mir-196a-2 Gastric Neoplasms 26345764 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overall, this meta-analysis failed to detect an association between five common miR-146a gene polymorphisms and GC susceptibility. However, this does not necessarily completely rule out a correlation between miRNA polymorphisms and GC susceptibility. genetics_GWAS hsa-mir-196a-2 Gastric Neoplasms 26345790 disease of cellular proliferation DOID:10534 C16 D013274 137215 In summary, the results suggested that the miR-146a rs2910164 polymorphism was related to gastric cancer risk in Asians but not in Caucasians, and no distinct correlation seemed to exist between the miR-196a-2 rs11614913 polymorphism and the risk of gastric cancer. genetics_GWAS hsa-mir-196a-2 Gastric Neoplasms 19834808 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-196a-2:Association of microRNA-196a-2 gene polymorphism with gastric cancer risk genetics_GWAS hsa-mir-196a-2 Gastric Neoplasms 23975664 disease of cellular proliferation DOID:10534 C16 D013274 137215 Prognostic role of microRNA polymorphisms in advanced gastric cancer: a translational study of the Arbeitsgemeinschaft Internistische Onkologie (AIO). genetics_GWAS hsa-mir-200c Gastric Neoplasms 23065816 disease of cellular proliferation DOID:10534 C16 D013274 137215 G-A variant in miR-200c binding site of EFNA1 alters susceptibility to gastric cancer genetics_GWAS hsa-mir-212 Gastric Neoplasms 24981235 disease of cellular proliferation DOID:10534 C16 D013274 137215 A functional variant at miR-132-3p, miR-212-3p, and miR-361-5p binding site in CD80 gene alters susceptibility to gastric cancer in a Chinese Han population. genetics_GWAS hsa-mir-214 Gastric Neoplasms 25998065 disease of cellular proliferation DOID:10534 C16 D013274 137215 Our data suggested that rs114673809, which is located at the miR-214 binding site in the 3'-UTR of MTHFR, may play an important role in the development of gastric cancer in a Chinese Han population. genetics_GWAS hsa-mir-219-1 Gastric Neoplasms 23975664 disease of cellular proliferation DOID:10534 C16 D013274 137215 Prognostic role of microRNA polymorphisms in advanced gastric cancer: a translational study of the Arbeitsgemeinschaft Internistische Onkologie (AIO). genetics_GWAS hsa-mir-26a-1 Gastric Neoplasms 23975664 disease of cellular proliferation DOID:10534 C16 D013274 137215 Prognostic role of microRNA polymorphisms in advanced gastric cancer: a translational study of the Arbeitsgemeinschaft Internistische Onkologie (AIO). genetics_GWAS hsa-mir-27a Gastric Neoplasms 25399405 disease of cellular proliferation DOID:10534 C16 D013274 137215 rs895819 and rs11671784 inversely affect gastric cancer risk and the influence was closely related to their effects on miR-27a expression. genetics_GWAS hsa-mir-27a Gastric Neoplasms 25795117 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-27a rs895819 and miR-149 rs2292832 are of potential forewarning ability for gastric cancer risk. genetics_GWAS hsa-mir-27a Gastric Neoplasms 26345764 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overall, this meta-analysis failed to detect an association between five common miR-146a gene polymorphisms and GC susceptibility. However, this does not necessarily completely rule out a correlation between miRNA polymorphisms and GC susceptibility. genetics_GWAS hsa-mir-27a Gastric Neoplasms 23975664 disease of cellular proliferation DOID:10534 C16 D013274 137215 Prognostic role of microRNA polymorphisms in advanced gastric cancer: a translational study of the Arbeitsgemeinschaft Internistische Onkologie (AIO). genetics_GWAS hsa-mir-27a Gastric Neoplasms 20666778 disease of cellular proliferation DOID:10534 C16 D013274 137215 mir-27a:mir-27a genetic variant contributes to gastric cancer susceptibility genetics_GWAS hsa-mir-27a Gastric Neoplasms 22350505 disease of cellular proliferation DOID:10534 C16 D013274 137215 The SNP rs895819 in the miR-27a gene with the minor allele C presented significantly reduced risk to gastric cancer in Chinese population. genetics_GWAS hsa-mir-27a Gastric Neoplasms 23246964 disease of cellular proliferation DOID:10534 C16 D013274 137215 Genetic variations in miR-27a gene decrease mature miR-27a level and reduce gastric cancer susceptibility genetics_GWAS hsa-mir-29c Gastric Neoplasms 25661340 disease of cellular proliferation DOID:10534 C16 D013274 137215 A miR-29c binding site genetic variant in the 3'-untranslated region of LAMTOR3 gene is associated with gastric cancer risk. genetics_GWAS hsa-mir-30c-1 Gastric Neoplasms 22108846 disease of cellular proliferation DOID:10534 C16 D013274 137215 The genotype frequencies of pre-miR-30c A/G (Polymorphism rs928508 in pre-miR-30c) in gastric cancer patients were obviously different from those in the controls (P = 0.022). AA genotype carriers were associated with an increased risk of gastric cancer compared with GG genotype (adjusted odds ratio (OR) = 1.83, 95% confidence interval (CI): 1.07-3.15, P = 0.029). Moreover, the gastric cancer risk especially elevated in older individuals (aged >60 years), males, nonsmokers, and Helicobacter pylori (H. pylori)-infected individuals (adjusted OR = 2.66, 95% CI: 1.38-5.13, P = 0.004; adjusted OR = 1.90, 95% CI: 1.10-3.27, P = 0.022; adjusted OR = 1.94, 95% CI: 1.12-3.35, P = 0.018; adjusted OR = 1.83, 95% CI: 1.08-3.10, P = 0.024, respectively). Further stratified analysis indicated that AA genotype facilitated developing of gastric cancer with lymph node metastasis (adjusted OR = 2.23, 95% CI: 1.07-4.64, P = 0.032). Expression analysis detected that rs928508 AA showed a significantly increased level of mature miR-30c compared with GG or AG/GG genotype (P = 0.011 or P = 0.013). Patients with AA genotype were associated with unfavorable outcome in overall survival compared with AG/GG genotype (Log rank 5.848, P = 0.016). This study demonstrates that pre-miR-30c A/G polymorphism may be associated with an increased risk of gastric cancer in a Chinese population through altering mature miR-30c expression. genetics_GWAS hsa-mir-30c-2 Gastric Neoplasms 22108846 disease of cellular proliferation DOID:10534 C16 D013274 137215 The genotype frequencies of pre-miR-30c A/G (Polymorphism rs928508 in pre-miR-30c) in gastric cancer patients were obviously different from those in the controls (P = 0.022). AA genotype carriers were associated with an increased risk of gastric cancer compared with GG genotype (adjusted odds ratio (OR) = 1.83, 95% confidence interval (CI): 1.07-3.15, P = 0.029). Moreover, the gastric cancer risk especially elevated in older individuals (aged >60 years), males, nonsmokers, and Helicobacter pylori (H. pylori)-infected individuals (adjusted OR = 2.66, 95% CI: 1.38-5.13, P = 0.004; adjusted OR = 1.90, 95% CI: 1.10-3.27, P = 0.022; adjusted OR = 1.94, 95% CI: 1.12-3.35, P = 0.018; adjusted OR = 1.83, 95% CI: 1.08-3.10, P = 0.024, respectively). Further stratified analysis indicated that AA genotype facilitated developing of gastric cancer with lymph node metastasis (adjusted OR = 2.23, 95% CI: 1.07-4.64, P = 0.032). Expression analysis detected that rs928508 AA showed a significantly increased level of mature miR-30c compared with GG or AG/GG genotype (P = 0.011 or P = 0.013). Patients with AA genotype were associated with unfavorable outcome in overall survival compared with AG/GG genotype (Log rank 5.848, P = 0.016). This study demonstrates that pre-miR-30c A/G polymorphism may be associated with an increased risk of gastric cancer in a Chinese population through altering mature miR-30c expression. genetics_GWAS hsa-mir-34b Gastric Neoplasms 25190020 disease of cellular proliferation DOID:10534 C16 D013274 137215 Promoter polymorphisms of miR-34b/c are associated with risk of gastric cancer in a Chinese population. genetics_GWAS hsa-mir-34b Gastric Neoplasms 25658980 disease of cellular proliferation DOID:10534 C16 D013274 137215 rs4938723 polymorphism is associated with a decreased risk of gastric cancer. genetics_GWAS hsa-mir-34c Gastric Neoplasms 25190020 disease of cellular proliferation DOID:10534 C16 D013274 137215 Promoter polymorphisms of miR-34b/c are associated with risk of gastric cancer in a Chinese population. genetics_GWAS hsa-mir-34c Gastric Neoplasms 25658980 disease of cellular proliferation DOID:10534 C16 D013274 137215 rs4938723 polymorphism is associated with a decreased risk of gastric cancer. genetics_GWAS hsa-mir-361 Gastric Neoplasms 24981235 disease of cellular proliferation DOID:10534 C16 D013274 137215 A functional variant at miR-132-3p, miR-212-3p, and miR-361-5p binding site in CD80 gene alters susceptibility to gastric cancer in a Chinese Han population. genetics_GWAS hsa-mir-423 Gastric Neoplasms 23975664 disease of cellular proliferation DOID:10534 C16 D013274 137215 Prognostic role of microRNA polymorphisms in advanced gastric cancer: a translational study of the Arbeitsgemeinschaft Internistische Onkologie (AIO). genetics_GWAS hsa-mir-449a Gastric Neoplasms 26722545 disease of cellular proliferation DOID:10534 C16 D013274 137215 In conclusion, our findings suggest that miR-449a rs112310158 is a genetic risk factor for GC. genetics_GWAS hsa-mir-499 Gastric Neoplasms 24107911 disease of cellular proliferation DOID:10534 C16 D013274 137215 The rs3746444 (A>G) SNP is not associated with susceptibility to GC in the Chinese population. genetics_GWAS hsa-mir-499 Gastric Neoplasms 25795117 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-27a rs895819 and miR-149 rs2292832 are of potential forewarning ability for gastric cancer risk. genetics_GWAS hsa-mir-499 Gastric Neoplasms 26345764 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overall, this meta-analysis failed to detect an association between five common miR-146a gene polymorphisms and GC susceptibility. However, this does not necessarily completely rule out a correlation between miRNA polymorphisms and GC susceptibility. genetics_GWAS hsa-mir-499 Gastric Neoplasms 26597478 disease of cellular proliferation DOID:10534 C16 D013274 137215 The present study indicated that miR-499 rs3746444 might contribute to GC risk and this SNP could be developed as a biomarker for GC prediction. genetics_GWAS hsa-mir-505 Gastric Neoplasms 26394032 disease of cellular proliferation DOID:10534 C16 D013274 137215 The PSMD10 rs111638916 SNP is highly associated with an increased risk of GC in Chinese patients, and could serve as a novel biomarker for this disease. genetics_GWAS hsa-mir-570 Gastric Neoplasms 22190470 disease of cellular proliferation DOID:10534 C16 D013274 137215 A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding. genetics_GWAS hsa-mir-605 Gastric Neoplasms 21976437 disease of cellular proliferation DOID:10534 C16 D013274 137215 Marginally significant associations were found both for hsa-miR-149 rs2292832 with gastric cancer risk (TC+CC vs. TT, OR=0.68, 95% CI: 0.44-1.04) and for hsa-miR-605 rs2043556 with colorectal cancer risk (AG+GG vs. AA, OR=0.70, 95% CI: 0.48-1.02) in males. genetics_GWAS hsa-mir-624 Gastric Neoplasms 24568522 disease of cellular proliferation DOID:10534 C16 D013274 137215 Bioinformatic prediction of SNPs within miRNA binding sites of inflammatory genes associated with gastric cancer. genetics_GWAS hsa-mir-938 Gastric Neoplasms 22537748 disease of cellular proliferation DOID:10534 C16 D013274 137215 Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer. genetics_GWAS hsa-mir-146a Gastrointestinal Neoplasms 25693929 D37.9 D005770 No significant association between miR-146a rs2910164G/C polymorphism and gastrointestinal cancer susceptibility was found in this meta-analysis. But for homozygous model, people with GG genotype may have increased risk of developing colorectal cancer. genetics_GWAS hsa-mir-146a Gastrointestinal Neoplasms 20653068 D37.9 D005770 Pre-miR-146a C/G polymorphism might be associated with an elevatedrisk of gastric cancer in Chinese population. genetics_GWAS hsa-mir-146a Gastrointestinal Neoplasms 20721625 D37.9 D005770 This study revealed the combined effect of miR-146a rs2910164 G/G and TLR4 +3725 C allele on the increased risk of severe gastric atrophy among the H. pylori-infected Japanese subjects. genetics_GWAS hsa-mir-146a Gastrointestinal Neoplasms 21073609 D37.9 D005770 The rs2910164 (G>C) SNP in the miR-146a is associated with susceptibility to GC. genetics_GWAS hsa-mir-146a Generalized Epilepsy with Febrile Seizures Plus 25319229 nervous system disease DOID:0060170 G40.3 C565808 604233 Association of genetic polymorphism of pre-microRNA-146a rs2910164 and serum high-mobility group box 1 with febrile seizures in Egyptian children. genetics_GWAS hsa-mir-182 Glaucoma 27537254 nervous system disease DOID:1686 H40 D005901 137750 A Common Variant in MIR182 Is Associated With Primary Open-Angle Glaucoma in the NEIGHBORHOOD Consortium. genetics_GWAS hsa-mir-5481 Glaucoma 25809640 nervous system disease DOID:1686 H40 D005901 137750 These data support the role of hsa-miR-548l as a regulator of FOXC1 translation and provide evidence for the c.*734A>T variant as a modifier factor for the activity of coding glaucoma-associated FOXC1 mutations. genetics_GWAS hsa-mir-146a Glioblastoma 21744077 D005909 HP:0100843 A functional polymorphism in the pre-miR-146a gene is associated with risk and prognosis in adult glioma. An increased glioma risk was observed among rs2910164 minor allele (C) carriers (per allele OR (95%CI)=1.22 (1.01-1.46, p (trend)=0.039)). The association was stronger among older subjects carrying at least one copy of the C allele (OR (95% CI)=1.38 (1.04-1.83, P=0.026). Mortality was increased among minor allele carriers (HR(95% CI)=1.33 (1.03-1.72, P=0.029)), with the association largely restricted to females (HR (95% CI)=2.02 (1.28-3.17, P=0.002)). genetics_GWAS hsa-mir-196a-1 Glioma 20229273 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 A polymorphism of microRNA196a genome region was associated with decreased risk of glioma in Chinese population genetics_GWAS hsa-mir-196a2 Glioma 27796868 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Effect of rs11614913 Polymorphism on Mature miR196a2 Expression and its Target Gene HOXC8 Expression in Human Glioma. genetics_GWAS hsa-mir-196a-2 Glioma 20229273 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 A polymorphism of microRNA196a genome region was associated with decreased risk of glioma in Chinese population genetics_GWAS hsa-mir-1207 Glomerulonephritis 22319602 urinary system disease DOID:2921 N05 D005921 305800 HP:0000099 A miR-1207-5p binding site polymorphism (C1936T, rs13385) abolishes regulation of HBEGF and is associated with disease severity in CFHR5 nephropathy. genetics_GWAS hsa-mir-519a-1 Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-519a-2 Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-519b Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-519c Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-519d Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-519e Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-520a Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-520b Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-520d Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-520e Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-520f Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-520g Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-520h Gout 21558165 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520. genetics_GWAS hsa-mir-146a Graft-Versus-Host Disease 27156151 D89.813 D006086 614395 expression levels of miR-146aC>G, miR-196a2T>C and putative gene-gene interaction between miR-146a, miR-196a2, miR-149 may be involved in RIF development in Korean women. genetics_GWAS hsa-mir-149 Graft-Versus-Host Disease 27156151 D89.813 D006086 614395 expression levels of miR-146aC>G, miR-196a2T>C and putative gene-gene interaction between miR-146a, miR-196a2, miR-149 may be involved in RIF development in Korean women. genetics_GWAS hsa-mir-196a2 Graft-Versus-Host Disease 27156151 D89.813 D006086 614395 expression levels of miR-146aC>G, miR-196a2T>C and putative gene-gene interaction between miR-146a, miR-196a2, miR-149 may be involved in RIF development in Korean women. genetics_GWAS hsa-mir-499a Graft-Versus-Host Disease 27156151 D89.813 D006086 614395 expression levels of miR-146aC>G, miR-196a2T>C and putative gene-gene interaction between miR-146a, miR-196a2, miR-149 may be involved in RIF development in Korean women. genetics_GWAS hsa-mir-125a Habitual Abortion 21788734 N96 D000026 Two common SNPs (rs41275794, rs12976445) in pri-miR-125a alter the mature miRNA expression and associate with Abortion, Habitual in a Han-Chinese population. genetics_GWAS hsa-mir-196a-2 Habitual Abortion 22222140 N96 D000026 RSA(recurrent spontaneous abortion) patients exhibited significantly different frequencies of the miR-196a2CC (TT+TC vs. CC; adjusted odds ratio [AOR], 1.587; 95% confidence interval [CI], 1.042-2.417) and miR-499AG+GG genotypes (AOR, 1.671; 95% CI, 1.054-2.651) compared with the control group. genetics_GWAS hsa-mir-499a Habitual Abortion 22222140 N96 D000026 RSA(recurrent spontaneous abortion) patients exhibited significantly different frequencies of the miR-196a2CC (TT+TC vs. CC; adjusted odds ratio [AOR], 1.587; 95% confidence interval [CI], 1.042-2.417) and miR-499AG+GG genotypes (AOR, 1.671; 95% CI, 1.054-2.651) compared with the control group. genetics_GWAS hsa-mir-146a Head And Neck Neoplasms 26277865 disease of cellular proliferation DOID:11934 C76.0 D006258 HP:0012288 Significant association between functional microRNA polymorphisms and head and neck cancer susceptibility: a comprehensive meta-analysis. genetics_GWAS hsa-mir-149 Head And Neck Neoplasms 26277865 disease of cellular proliferation DOID:11934 C76.0 D006258 HP:0012288 Significant association between functional microRNA polymorphisms and head and neck cancer susceptibility: a comprehensive meta-analysis. genetics_GWAS hsa-mir-196a-2 Head And Neck Neoplasms 26277865 disease of cellular proliferation DOID:11934 C76.0 D006258 HP:0012288 Significant association between functional microRNA polymorphisms and head and neck cancer susceptibility: a comprehensive meta-analysis. genetics_GWAS hsa-mir-499 Head And Neck Neoplasms 26277865 disease of cellular proliferation DOID:11934 C76.0 D006258 HP:0012288 Significant association between functional microRNA polymorphisms and head and neck cancer susceptibility: a comprehensive meta-analysis. genetics_GWAS hsa-mir-885 Head And Neck Neoplasms 23271051 disease of cellular proliferation DOID:11934 C76.0 D006258 HP:0012288 A functional variant at the miR-885-5p binding site of CASP3 confers risk of both index and second primary malignancies in patients with head and neck cancer genetics_GWAS hsa-mir-22 Heart Failure 23372812 I50 D006331 HP:0001635 Common variation neighbouring micro-RNA 22 is associated with increased left ventricular mass. genetics_GWAS hsa-mir-499a Heart Failure 22374132 I50 D006331 HP:0001635 A naturally occurring miR-499 mutation(u17c in the 3' end) outside the critical seed sequence modifies mRNA targeting and end-organ function. genetics_GWAS hsa-let-7 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-146 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-150 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-155 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-15a Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-16-1 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-21 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-221 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-222 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-29 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-34 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-372 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-373 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-mir-708 Hematologic Neoplasms 26520014 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 our compiled results will be valuable for researchers interested in determining the role of target-SNPs in the development of hematological malignancies. genetics_GWAS hsa-let-7 Hepatitis B Virus Infection 24729511 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association of a functional RAD52 genetic variant locating in a miRNA binding site with risk of HBV-related hepatocellular carcinoma. genetics_GWAS hsa-let-7c Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-106b Hepatitis B Virus Infection 22393390 disease by infectious agent DOID:2043 B16/18 D006509 610424 A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)=0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR=1.25, 95% CIs=1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues. genetics_GWAS hsa-mir-106b Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-122 Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-124 Hepatitis B Virus Infection 23807362 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association between microRNA polymorphisms and humoral immunity to hepatitis B vaccine. genetics_GWAS hsa-mir-146a Hepatitis B Virus Infection 23292505 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association of a single-nucleotide polymorphism within the miR-146a gene with susceptibility for acute-on-chronic hepatitis B liver failure genetics_GWAS hsa-mir-146a Hepatitis B Virus Infection 23807362 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association between microRNA polymorphisms and humoral immunity to hepatitis B vaccine. genetics_GWAS hsa-mir-146a Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-149 Hepatitis B Virus Infection 23807362 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association between microRNA polymorphisms and humoral immunity to hepatitis B vaccine. genetics_GWAS hsa-mir-149 Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-196a-1 Hepatitis B Virus Infection 23516510 disease by infectious agent DOID:2043 B16/18 D006509 610424 Associations of pri-miR-34b/c and pre-miR-196a2 Polymorphisms and Their Multiplicative Interactions with Hepatitis B Virus Mutations with Hepatocellular Carcinoma Risk genetics_GWAS hsa-mir-196a-2 Hepatitis B Virus Infection 23807362 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association between microRNA polymorphisms and humoral immunity to hepatitis B vaccine. genetics_GWAS hsa-mir-196a-2 Hepatitis B Virus Infection 23516510 disease by infectious agent DOID:2043 B16/18 D006509 610424 Associations of pri-miR-34b/c and pre-miR-196a2 Polymorphisms and Their Multiplicative Interactions with Hepatitis B Virus Mutations with Hepatocellular Carcinoma Risk genetics_GWAS hsa-mir-196a-2 Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-218 Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-25 Hepatitis B Virus Infection 22393390 disease by infectious agent DOID:2043 B16/18 D006509 610424 A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)=0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR=1.25, 95% CIs=1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues. genetics_GWAS hsa-mir-26a-1 Hepatitis B Virus Infection 23807362 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association between microRNA polymorphisms and humoral immunity to hepatitis B vaccine. genetics_GWAS hsa-mir-27a Hepatitis B Virus Infection 23807362 disease by infectious agent DOID:2043 B16/18 D006509 610424 Association between microRNA polymorphisms and humoral immunity to hepatitis B vaccine. genetics_GWAS hsa-mir-34b Hepatitis B Virus Infection 23516510 disease by infectious agent DOID:2043 B16/18 D006509 610424 Associations of pri-miR-34b/c and pre-miR-196a2 Polymorphisms and Their Multiplicative Interactions with Hepatitis B Virus Mutations with Hepatocellular Carcinoma Risk genetics_GWAS hsa-mir-34b Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-34c Hepatitis B Virus Infection 23516510 disease by infectious agent DOID:2043 B16/18 D006509 610424 Associations of pri-miR-34b/c and pre-miR-196a2 Polymorphisms and Their Multiplicative Interactions with Hepatitis B Virus Mutations with Hepatocellular Carcinoma Risk genetics_GWAS hsa-mir-34c Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-499 Hepatitis B Virus Infection 25966251 disease by infectious agent DOID:2043 B16/18 D006509 610424 The meta-analysis results indicated that the miR-196a-2*T,miR-122*del, miR-106b-25*A, and miR-let-7c*del alleles/carriers increase the risk of hepatitis B among the Asian population. However, the miR-146a, miR- 499,miR-149, miR-218, and miR-34b/c polymorphisms may not be linked with the risk of hepatitis B. Further investigations are warranted to determine the exact associations between microRNA mutations and hepatitis B susceptibility. genetics_GWAS hsa-mir-196a-2 Hepatitis C Virus Infection 21604580 disease by infectious agent DOID:1883 B19.2 D006526 609532 SNP rs11614913 on miR196a-2 gene is associated with the antiviral therapy efficacy of hepatitis C patients.The TT genotype or T alleles be associated with the SVR while the CC genotype or C allele could be related to the NVR or recurrence. genetics_GWAS hsa-mir-146a Hirschsprung Disease 25445498 gastrointestinal system disease DOID:10487 Q43.1 D006627 600156 HP:0002251 the polymorphism rs2910164 in pre-miR-146a might alter the production of mature miR-146a and then down-regulate the target gene ROBO1, which plays an important role in pathogenesis of HSCR. genetics_GWAS hsa-mir-27a Human Immunodeficiency Virus Infection 27919232 B20 D015658 609423 microRNA-27a rs895819 is associated with obesity in HIV infected preeclamptic Black South African women on HAART. genetics_GWAS hsa-mir-182 Hyperactivity Disorder 23906647 disease of mental health DOID:1094 F90 D001289 143465 HP:0007018 Evaluation of single nucleotide polymorphisms in the miR-183-96-182 cluster in adulthood attention-deficit and hyperactivity disorder (ADHD) and substance use disorders (SUDs). genetics_GWAS hsa-mir-183 Hyperactivity Disorder 23906647 disease of mental health DOID:1094 F90 D001289 143465 HP:0007018 Evaluation of single nucleotide polymorphisms in the miR-183-96-182 cluster in adulthood attention-deficit and hyperactivity disorder (ADHD) and substance use disorders (SUDs). genetics_GWAS hsa-mir-96 Hyperactivity Disorder 23906647 disease of mental health DOID:1094 F90 D001289 143465 HP:0007018 Evaluation of single nucleotide polymorphisms in the miR-183-96-182 cluster in adulthood attention-deficit and hyperactivity disorder (ADHD) and substance use disorders (SUDs). genetics_GWAS hsa-mir-33b Hyperglycemia 24825092 disease of metabolism DOID:4195 E78.1 D006943 HP:0003074 Association of rs8066560 variant in the sterol regulatory element-binding protein 1 (SREBP-1) and miR-33b genes with hyperglycemia and insulin resistance. genetics_GWAS hsa-mir-485 Hyperglycemia 24387992 disease of metabolism DOID:4195 E78.1 D006943 HP:0003074 An APOA5 3' UTR variant associated with plasma triglycerides triggers APOA5 downregulation by creating a functional miR-485-5p binding site. genetics_GWAS hsa-mir-122 Hypertension 19067360 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 a polymorphism of the 3'UTR of the SLC7A1 gene affects the binding with miR-122 genetics_GWAS hsa-mir-146a Hypertension 27379568 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 This study suggests that the variant of miR-146aC>G polymorphism and allelic combinations, at least in Koreans, affect susceptibility to hypertension. genetics_GWAS hsa-mir-155 Hypertension 20966899 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 The interplay between miR-155 expression, +1166C polymorphism, and AT1R protein expression may have a role in the regulation of blood pressure. genetics_GWAS hsa-mir-31 Hypertension 23943853 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 Human angiotensinogen +11525 C/A polymorphism modulates its gene expression through microRNA binding. genetics_GWAS hsa-mir-518 Hypertension 24687999 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 Our results suggest that TGFBR2 and miR-518 harbor variants that increase the risk of EH and affect blood pressure homeostasis as well as efficacy of antihypertensive agents. genetics_GWAS hsa-mir-584 Hypertension 23943853 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 Human angiotensinogen +11525 C/A polymorphism modulates its gene expression through microRNA binding. genetics_GWAS hsa-mir-637 Hypertension 21558123 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 A common genetic variant (rs938671) in the 3'-UTR of Vacuolar H+-ATPase ATP6V0A1 creates a micro-RNA (hsa-miR-637) motif to alter Chromogranin A (CHGA) processing and hypertension risk. genetics_GWAS hsa-mir-637 Hypertension 21846868 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 ATP6V0A1 Polymorphism and MicroRNA-637 may have A Pathogenetic Role for MicroRNAs in Essential Hypertension. genetics_GWAS hsa-mir-155 Hypertrophy 21771600 D006984 the C allele of rs5186 was associated with a significant increase in SWT (p=0.003) and LVM (p=0.001). This functional polymorphism increases expression of AGTR1 by altering the binding site for miR-155 genetics_GWAS hsa-mir-146a IgA Nephropathy 24781267 urinary system disease DOID:2986 N02.8 D005922 161950 HP:0000794 These results indicated that rs2910164 may affect the susceptibility and severity of pediatric IgAN. Further studies are needed to validate these findings. genetics_GWAS hsa-mir-146a Immune Thrombocytopenic Purpura 24502829 immune system disease DOID:8924 D69.3 D016553 188030 hsa-mir-146a rs2910164 polymorphism and risk of immune thrombocytopenia. genetics_GWAS hsa-mir-146a Intracranial Aneurysm 26214448 cardiovascular system disease DOID:10941 I67.1 D002532 105800 Association between the hsa-miR-146a rs2910164 functional polymorphism with susceptibility to intracranial aneurysm. genetics_GWAS hsa-mir-34b Intracranial Aneurysm 22844323 cardiovascular system disease DOID:10941 I67.1 D002532 105800 The CC genotype of miR-34b/c rs4938723 was significantly associated with a decreased risk of IA compared with the TT genotype. Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes. genetics_GWAS hsa-mir-34c Intracranial Aneurysm 22844323 cardiovascular system disease DOID:10941 I67.1 D002532 105800 The CC genotype of miR-34b/c rs4938723 was significantly associated with a decreased risk of IA compared with the TT genotype. Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes. genetics_GWAS hsa-mir-510 Irritable Bowel Syndrome 18614545 syndrome DOID:9778 K58 D043183 First evidence for an association of a functional variant in the microRNA-510 target site of the serotonin receptor type 3E gene with diarrhea predominant irritable bowel syndrome. genetics_GWAS hsa-mir-146a Kaposi Sarcoma 27819716 disease of cellular proliferation DOID:8632 C46 D012514 Association of genetic variations in miR-146a rs2910164 and miR-149 rs11614913 with the development of classic Kaposi sarcoma. genetics_GWAS hsa-mir-149 Kaposi Sarcoma 27819716 disease of cellular proliferation DOID:8632 C46 D012514 Association of genetic variations in miR-146a rs2910164 and miR-149 rs11614913 with the development of classic Kaposi sarcoma. genetics_GWAS hsa-mir-146a Kidney Diseases [unspecific] 26426696 N18.9 D007674 There was no association of rs2910164 with susceptibility to IgAN in adults from a Chinese Han population. However, rs2910164 was correlated with the age of onset of IgAN in adult patients. genetics_GWAS hsa-mir-146a Leprosy 25187983 disease by infectious agent DOID:1024 A30.9 D007918 609888 Pre-miR-146a (rs2910164 G>C) single nucleotide polymorphism is genetically and functionally associated with leprosy. genetics_GWAS hsa-mir-142 Leukemia 15737576 C95 D007938 613065 HP:0001909 Some human miRNAs are linked to leukemias: the miR-15a/miR-16 locus is frequently deleted or down-regulated in patients with B-cell chronic lymphocytic leukemia and miR-142 is at a translocation site found in a case of aggressive B-cell leukemia. genetics_GWAS hsa-mir-125b-1 Leukemia, Biphenotypic, Acute 20485370 disease of cellular proliferation DOID:9953 C95.0 D015456 HP:0005531 miR-125b-1:A new recurrent translocation t(11;14)(q24;q32) involving IGH@ and miR-125b-1 in B-cell progenitor acute lymphoblastic leukemia genetics_GWAS hsa-mir-499 Leukemia, Lymphoblastic, Acute 24618566 disease of cellular proliferation DOID:9952 C91.0 D054198 247640 HP:0006721 We found 11 SNPs significantly associated with ALL susceptibility. These included three SNPs present in miRNA genes (miR-612, miR-499, and miR-449b) and eight SNPs present in six miRNA biogenesis pathway genes (TNRC6B, DROSHA, DGCR8, EIF2C1, CNOT1, and CNOT6). genetics_GWAS hsa-mir-34b Leukemia, Lymphoblastic, Acute, Childhood 27886674 disease of cellular proliferation DOID:0080144 C91.0 D054198 613065 Pri-miR-34b/c rs4938723 polymorphism is associated with the risk of childhood acute lymphoblastic leukemia. genetics_GWAS hsa-mir-34c Leukemia, Lymphoblastic, Acute, Childhood 27886674 disease of cellular proliferation DOID:0080144 C91.0 D054198 613065 Pri-miR-34b/c rs4938723 polymorphism is associated with the risk of childhood acute lymphoblastic leukemia. genetics_GWAS hsa-mir-1206 Leukemia, Lymphocytic, Chronic, B-Cell 25793711 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 These findings suggest that polymorphisms in genes involved in miRNAs biogenesis pathway as well as in pre-miRNAs contribute to the risk of CLL. Large-scale studies are needed to validate the current findings. genetics_GWAS hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 16251535 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 mutation genetics_GWAS hsa-mir-187 Leukemia, Lymphocytic, Chronic, B-Cell 16251535 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 mutation genetics_GWAS hsa-mir-196a-2 Leukemia, Lymphocytic, Chronic, B-Cell 25793711 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 These findings suggest that polymorphisms in genes involved in miRNAs biogenesis pathway as well as in pre-miRNAs contribute to the risk of CLL. Large-scale studies are needed to validate the current findings. genetics_GWAS hsa-mir-206 Leukemia, Lymphocytic, Chronic, B-Cell 16251535 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 mutation genetics_GWAS hsa-mir-27b Leukemia, Lymphocytic, Chronic, B-Cell 16251535 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 mutation genetics_GWAS hsa-mir-29b-1 Leukemia, Lymphocytic, Chronic, B-Cell 16251535 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 mutation genetics_GWAS hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 26959643 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 mutations in the mir-15a/16-1 loci are responsible for decreased expression genetics_GWAS hsa-mir-34c Leukemia, Myeloid 24886876 disease of cellular proliferation DOID:8692 C92 D007951 HP:0012324 Our study implicates that microRNA-binding site polymorphisms modulate leukemia risk by interfering with the miRNA-mediated regulation. Our findings underscore the significance of variability in 3' untranslated regions in leukemia. genetics_GWAS hsa-mir-449b Leukemia, Myeloid 24886876 disease of cellular proliferation DOID:8692 C92 D007951 HP:0012324 Our study implicates that microRNA-binding site polymorphisms modulate leukemia risk by interfering with the miRNA-mediated regulation. Our findings underscore the significance of variability in 3' untranslated regions in leukemia. genetics_GWAS hsa-mir-125b-1 Leukemia, Myeloid, Acute 22843432 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 MicroRNA-125b-1 accelerates a C-terminal mutant of C/EBPα (C/EBPα-C(m))-induced myeloid leukemia. genetics_GWAS hsa-mir-142 Leukemia, Myeloid, Acute 24724784 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Absence of miR-142 mutation in Chinese patients with acute myeloid leukemia. genetics_GWAS hsa-mir-337 Leukemia, Myeloid, Acute 23065518 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 A polymorphism in the 3'-untranslated region of the NPM1 gene causes illegitimate regulation by microRNA-337-5p and correlates with adverse outcome in acute myeloid leukemia genetics_GWAS hsa-mir-370 Leukemia, Myeloid, Acute 23077663 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Integration of SNP and mRNA arrays with microRNA profiling reveals that MiR-370 is upregulated and targets NF1 in acute myeloid leukemia genetics_GWAS hsa-mir-126 Leukemia-Lymphoma, Precursor T-Cell Lymphoblastic 20621067 disease of cellular proliferation DOID:5599 C83.5 D054218 miR-126:Alteration of processing induced by a single nucleotide polymorphism in pri-miR-126 genetics_GWAS hsa-mir-128-2 Leukemia-Lymphoma, Precursor T-Cell Lymphoblastic 20237425 disease of cellular proliferation DOID:5599 C83.5 D054218 A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells. genetics_GWAS hsa-mir-605 Li-Fraumeni Syndrome 25683625 genetic disease DOID:3012 Z15.01 D016864 151623 A functional variant in miR-605 modifies the age of onset in Li-Fraumeni syndrome. genetics_GWAS hsa-let-7 Liver Cirrhosis 27992614 endocrine system disease DOID:5082 K74 D008103 215600 HP:0001394 A Single Nucleotide Polymorphism in the RASGRF2 Gene Is Associated with Alcoholic Liver Cirrhosis in Men. genetics_GWAS hsa-mir-196a-2 Liver Cirrhosis 26529280 endocrine system disease DOID:5082 K74 D008103 215600 HP:0001394 In summary, rs12304647 is associated with a reduced risk of progression to HCC in patients with chronic HBV infection. genetics_GWAS hsa-mir-196a-2 Liver Neoplasms 24633889 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 Quantitative assessment of the association between miR-196a2 rs11614913 polymorphism and cancer risk: evidence based on 45,816 subjects. genetics_GWAS hsa-let-7a-1 Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7a: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7a-2 Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7a: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7a-3 Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7a: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7b Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7b: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7c Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7c: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7d Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7d: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7e Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7e: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7f-1 Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7f: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7f-2 Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7f: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7g Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7g: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-let-7i Lung Neoplasms 18922928 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 let-7i: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk genetics_GWAS hsa-mir-146a Lung Neoplasms 25077922 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Effects of four single nucleotide polymorphisms in microRNA-coding genes on lung cancer risk. genetics_GWAS hsa-mir-146a Lung Neoplasms 25154761 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 MicroRNA-146a rs2910164 polymorphism is associated with susceptibility to non-small cell lung cancer in the Chinese population. genetics_GWAS hsa-mir-146a Lung Neoplasms 25524943 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 mir-196a2 SNP influences the susceptibility of lung cancer. Mir-146a and mir-149 SNP do not play a role in lung cancer risk. These findings need more validation by larger studies. genetics_GWAS hsa-mir-146a Lung Neoplasms 26083623 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The interactions between miRNA SNPs and cooking oil fume exposure suggested by ORs of different combination were not statistically significant. genetics_GWAS hsa-mir-146a Lung Neoplasms 26926727 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Rs11614913, rs12894467 and rs2910164 polymorphism were potentially associated with primary lung cancer in Fujian Han population. genetics_GWAS hsa-mir-146a Lung Neoplasms 24144839 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 These findings suggest that the rs2910164C>G in pre-miR-146a may contribute to genetic susceptibility to lung cancer, and that miR-146a might be involved in lung cancer development. genetics_GWAS hsa-mir-146a Lung Neoplasms 22818121 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Our findings suggest that polymorphisms in the rs2910164 of miR-146a and the rs11614913 of miR-196a2 are associated with prognosis in patients with completely resected NSCLC. genetics_GWAS hsa-mir-149 Lung Neoplasms 25077922 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Effects of four single nucleotide polymorphisms in microRNA-coding genes on lung cancer risk. genetics_GWAS hsa-mir-149 Lung Neoplasms 25524943 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 mir-196a2 SNP influences the susceptibility of lung cancer. Mir-146a and mir-149 SNP do not play a role in lung cancer risk. These findings need more validation by larger studies. genetics_GWAS hsa-mir-149 Lung Neoplasms 27685326 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 MicroRNA-149 rs2292832 polymorphism may not be associated with lung cancer risk in Chinese non-smoking female genetics_GWAS hsa-mir-196a Lung Neoplasms 22818121 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Our findings suggest that polymorphisms in the rs2910164 of miR-146a and the rs11614913 of miR-196a2 are associated with prognosis in patients with completely resected NSCLC. genetics_GWAS hsa-mir-196a-1 Lung Neoplasms 23143626 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Hsa-miR-196a2 functional SNP is associated with severe toxicity after platinum-based chemotherapy of advanced nonsmall cell lung cancer patients in a Chinese population genetics_GWAS hsa-mir-196a-2 Lung Neoplasms 26083623 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The interactions between miRNA SNPs and cooking oil fume exposure suggested by ORs of different combination were not statistically significant. genetics_GWAS hsa-mir-196a-2 Lung Neoplasms 26926727 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Rs11614913, rs12894467 and rs2910164 polymorphism were potentially associated with primary lung cancer in Fujian Han population. genetics_GWAS hsa-mir-196a-2 Lung Neoplasms 25077922 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Effects of four single nucleotide polymorphisms in microRNA-coding genes on lung cancer risk. genetics_GWAS hsa-mir-196a-2 Lung Neoplasms 25524943 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 mir-196a2 SNP influences the susceptibility of lung cancer. Mir-146a and mir-149 SNP do not play a role in lung cancer risk. These findings need more validation by larger studies. genetics_GWAS hsa-mir-196a-2 Lung Neoplasms 21483822 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 rs11614913 polymorphism:Overall, individuals with the TC/CC genotypes were associated with higher cancer risk than those with the TT genotype (OR=1.18, 95% CI=1.03-1.34, P<0.001 for heterogeneity test). In the stratified analyses, we observed that the CC genotype might modulate breast cancer risk (OR=1.11, 95%CI=1.01-1.23, P(heterogeneity)=0.210) and lung cancer risk (OR=1.25, 95%CI=1.06-1.46, P(heterogeneity)=0.958), comparing with the TC/TT genotype. Moreover, a significantly increased risk was found among Asian populations in a dominant model (TC/CC versus TT, OR=1.24, 95% CI=1.07-1.43, P(heterogeneity)=0.006). genetics_GWAS hsa-mir-196a-2 Lung Neoplasms 23143626 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Hsa-miR-196a2 functional SNP is associated with severe toxicity after platinum-based chemotherapy of advanced nonsmall cell lung cancer patients in a Chinese population genetics_GWAS hsa-mir-196a-2 Lung Neoplasms 18521189 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Therefore, the rs11614913 SNP in hsa-mir-196a2 may be a prognostic biomarker for NSCLC. genetics_GWAS hsa-mir-25 Lung Neoplasms 22349819 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 REV3L 3'UTR 460 T>C polymorphism in microRNA(miR-25/32) target sites contributes to lung cancer susceptibility. genetics_GWAS hsa-mir-26a-1 Lung Neoplasms 26926727 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Rs11614913, rs12894467 and rs2910164 polymorphism were potentially associated with primary lung cancer in Fujian Han population. genetics_GWAS hsa-mir-27a Lung Neoplasms 26083623 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The interactions between miRNA SNPs and cooking oil fume exposure suggested by ORs of different combination were not statistically significant. genetics_GWAS hsa-mir-27a Lung Neoplasms 26926727 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Rs11614913, rs12894467 and rs2910164 polymorphism were potentially associated with primary lung cancer in Fujian Han population. genetics_GWAS hsa-mir-300 Lung Neoplasms 26926727 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Rs11614913, rs12894467 and rs2910164 polymorphism were potentially associated with primary lung cancer in Fujian Han population. genetics_GWAS hsa-mir-30c-1 Lung Neoplasms 23159078 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Single nucleotide polymorphism in flanking region of miR-30c influences the maturing process of miR-30c in lung carcinoma genetics_GWAS hsa-mir-30c-2 Lung Neoplasms 23159078 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Single nucleotide polymorphism in flanking region of miR-30c influences the maturing process of miR-30c in lung carcinoma genetics_GWAS hsa-mir-32 Lung Neoplasms 22349819 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 REV3L 3'UTR 460 T>C polymorphism in microRNA(miR-25/32) target sites contributes to lung cancer susceptibility. genetics_GWAS hsa-mir-423 Lung Neoplasms 26083623 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The interactions between miRNA SNPs and cooking oil fume exposure suggested by ORs of different combination were not statistically significant. genetics_GWAS hsa-mir-423 Lung Neoplasms 26973201 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 These findings suggest that miR-146a rs2910164C>G and miR-423 rs6505162C>A polymorphisms may contribute to genetic susceptibility to lung cancer and lung adenocarcinoma in Chinese non-smoking females. genetics_GWAS hsa-mir-499 Lung Neoplasms 25614447 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 the rs3746444T>C polymorphism in mature miR-499 sequence could contribute to poor prognosis by modulating cancer-related genes' expression and thus involve tumorigenesis and anti-chemotherapy, which may be a useful biomarker to predict lung cancer patients' prognosis. genetics_GWAS hsa-mir-499b Lung Neoplasms 25077922 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Effects of four single nucleotide polymorphisms in microRNA-coding genes on lung cancer risk. genetics_GWAS hsa-mir-608 Lung Neoplasms 26083623 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The interactions between miRNA SNPs and cooking oil fume exposure suggested by ORs of different combination were not statistically significant. genetics_GWAS hsa-mir-629 Lung Neoplasms 22114071 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The rs2735383CC (NBS1 gene) genotype had a significantly increased risk of lung cancer under a recessive genetic model in the total 1559 cases versus 1679 controls (OR = 1.40, 95% C.I. = 1.18-1.66, P = 0.0001) when compared with GG or GC genotypes; the rs2735383CC genotype carriers had lower mRNA and protein expression levels in tumor tissues than those of other genotypes as qPCR and western blot shown. Luciferase assay revealed that the rs2735383C allele had a lower transcription activity than G allele; and the hsa-miR-629 but not hsa-miR-499-5P had effect on modulation of NBS1 gene in vitro. We further observed that the X-ray radiation induced more chromatid breaks in lymphocyte cells from the carriers of rs2735383CC homozygote than those from the subjects with other genotypes (P = 0.0008). Our data suggested that the rs2735383G>C variation contributes to an increased risk of lung cancer by diminishing gene's expression through binding of microRNA-629 to the polymorphic site in the 3'-UTR of NBS1 gene. genetics_GWAS hsa-mir-6720 Lymphedema 29511529 immune system disease DOID:4977 I89.0 D008209 PS153100 HP:0001004 rs121909106 and rs121909107 were predicted to have the most harmful effects, while hsa-miR-6886-5p, hsa-miR-6886-5p and hsa-miR-6720-3p were predicted to be the most important miRNAs affected genetics_GWAS hsa-mir-6886 Lymphedema 29511529 immune system disease DOID:4977 I89.0 D008209 PS153100 HP:0001004 rs121909106 and rs121909107 were predicted to have the most harmful effects, while hsa-miR-6886-5p, hsa-miR-6886-5p and hsa-miR-6720-3p were predicted to be the most important miRNAs affected genetics_GWAS hsa-mir-146a Lymphoma, B-Cell 25370733 disease of cellular proliferation DOID:707 D016393 109565 HP:0012191 MicroRNA-146a rs2910164 polymorphism and the risk of diffuse large B cell lymphoma in the Chinese Han population. genetics_GWAS hsa-mir-142 Lymphoma, Follicular 27389057 disease of cellular proliferation DOID:0050873 C82 D008224 613024 We found recurrent mutations of miR-142, which has not been previously been reported to be mutated in FL/tFL. genetics_GWAS hsa-mir-142 Lymphoma, Large B-Cell, Diffuse 27390358 disease of cellular proliferation DOID:0050745 C83.3 D016403 109565 Additionally, we detected recurrent mutations of hsa-miR-142 in diffuse large B-cell lymphomas and follicular lymphomas, and editing of the hsa-miR-376 cluster, providing evidence for microRNA editing in lymphomagenesis. genetics_GWAS hsa-mir-155 Lymphoma, Large B-Cell, Diffuse 25677902 disease of cellular proliferation DOID:0050745 C83.3 D016403 109565 the miRs expression in B-NHLs[11q] provides a new suggestion, in addition to pathomorphological and clinical similarities between classical, i.e.,MYC translocation-positive BL, and B-NHLs[11q], to recognize the B-NHLs[11q] subgroup of DLBCL/BL category as a MYC translocation-negative variant of BL in most cases, and points to the potential utility of miR-155/BIC/miR-21/miR-26a for the differential diagnosis of a heterogeneous category of DLBCL/BL. genetics_GWAS hsa-mir-21 Lymphoma, Large B-Cell, Diffuse 25677902 disease of cellular proliferation DOID:0050745 C83.3 D016403 109565 the miRs expression in B-NHLs[11q] provides a new suggestion, in addition to pathomorphological and clinical similarities between classical, i.e.,MYC translocation-positive BL, and B-NHLs[11q], to recognize the B-NHLs[11q] subgroup of DLBCL/BL category as a MYC translocation-negative variant of BL in most cases, and points to the potential utility of miR-155/BIC/miR-21/miR-26a for the differential diagnosis of a heterogeneous category of DLBCL/BL. genetics_GWAS hsa-mir-26a Lymphoma, Large B-Cell, Diffuse 25677902 disease of cellular proliferation DOID:0050745 C83.3 D016403 109565 the miRs expression in B-NHLs[11q] provides a new suggestion, in addition to pathomorphological and clinical similarities between classical, i.e.,MYC translocation-positive BL, and B-NHLs[11q], to recognize the B-NHLs[11q] subgroup of DLBCL/BL category as a MYC translocation-negative variant of BL in most cases, and points to the potential utility of miR-155/BIC/miR-21/miR-26a for the differential diagnosis of a heterogeneous category of DLBCL/BL. genetics_GWAS hsa-mir-376 Lymphoma, Large B-Cell, Diffuse 27390358 disease of cellular proliferation DOID:0050745 C83.3 D016403 109565 we detected recurrent mutations of hsa-miR-142 in diffuse large B-cell lymphomas and follicular lymphomas, and editing of the hsa-miR-376 cluster, providing evidence for microRNA editing in lymphomagenesis. genetics_GWAS hsa-mir-155 Lymphoma, Non-Hodgkin 22347493 disease of cellular proliferation DOID:0060060 C85.9 D008228 605027 HP:0012539 Variant rs928883, near miR-155, showed an association (OR per A-allele: 2.80 [95% CI: 1.63-4.82]; p(F)=0.027) with marginal zone lymphoma that is significant after correction for multiple testing. genetics_GWAS hsa-mir-196a Lymphoma, Non-Hodgkin 25501512 disease of cellular proliferation DOID:0060060 C85.9 D008228 605027 HP:0012539 the miR-196a2 polymorphism may increase the risk of NHL by altering the expression of mature miR-196a. genetics_GWAS hsa-mir-502 Lymphoma, Non-Hodgkin 25343552 disease of cellular proliferation DOID:0060060 C85.9 D008228 605027 HP:0012539 the SNP in the miRNA binding site of the SET8 3'-untranslated region seems to influence survival of NHL. It may have possible prognostic and survival value in the clinic. genetics_GWAS hsa-let-7 Macular Degeneration 28343170 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 miRNAs, single nucleotide polymorphisms (SNPs) and age-related macular degeneration (AMD). genetics_GWAS hsa-let-7a Macular Degeneration 28343170 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 miRNAs, single nucleotide polymorphisms (SNPs) and age-related macular degeneration (AMD). genetics_GWAS hsa-let-7b Macular Degeneration 28343170 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 miRNAs, single nucleotide polymorphisms (SNPs) and age-related macular degeneration (AMD). genetics_GWAS hsa-let-7d Macular Degeneration 28343170 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 miRNAs, single nucleotide polymorphisms (SNPs) and age-related macular degeneration (AMD). genetics_GWAS hsa-mir-146a Macular Degeneration 28343170 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 miRNAs, single nucleotide polymorphisms (SNPs) and age-related macular degeneration (AMD). genetics_GWAS hsa-mir-155 Macular Degeneration 28343170 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 miRNAs, single nucleotide polymorphisms (SNPs) and age-related macular degeneration (AMD). genetics_GWAS hsa-mir-1302-1 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-1302-2 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-1302-3 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-1302-4 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-1302-5 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-1302-6 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-1302-7 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-1302-8 Male Infertility 21601192 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro. genetics_GWAS hsa-mir-34b Male Infertility 26505368 reproductive system disease DOID:12336 N46.9 D007248 HP:0003251 Our results indicated that the MTHFR 3'-UTR rs55763075 polymorphism might modify the susceptibility to male infertility with idiopathic azoospermia. genetics_GWAS hsa-mir-103a-2 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-106b Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-1-1 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-133a-2 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-135b Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-137 Melanoma 21543894 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 miR-137 under expression was significantly associated with melanomas with the KRAS-variant. genetics_GWAS hsa-mir-146a Melanoma 23222547 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 The rs2910164 G>C polymorphism in microRNA-146a is associated with the incidence of malignant melanoma genetics_GWAS hsa-mir-146a Melanoma 26122011 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Association of microRNA 146a polymorphism rs2910164 and the risk of melanoma in an Italian population. genetics_GWAS hsa-mir-146a Melanoma 28654546 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Sex-specific effect of RNASEL rs486907 and miR-146a rs2910164 polymorphisms' interaction as a susceptibility factor for melanoma skin cancer. genetics_GWAS hsa-mir-151a Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-153-2 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-155 Melanoma 26068396 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Polymorphisms in 3'UTR of TYRP1 mRNA can affect TYRP1 mRNA regulation by miR-155 and its subsequent translation into protein. These SNPs can render TYRP1 mRNA and protein expression nonsusceptible to miR-155 activity and disclose a prognostic value for TYRP1 protein in a subgroup of melanoma patients. These data support the interest in the prognostic value of melanogenic markers and propose TYRP1 to refine prognosis in patients with advanced disease. genetics_GWAS hsa-mir-17 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-182 Melanoma 22752337 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Up-regulation of miR-182 expression after epigenetic modulation of human melanoma cells. genetics_GWAS hsa-mir-18a Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-194-1 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-199a-2 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-19a Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-19b-1 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-200a Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-200b Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-20a Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-214 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-215 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-218-1 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-219-1 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-221 Melanoma 21119596 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 This KIT variant results in a mismatch in the seed region of a miR-221 complementary site and reporter data suggests that this mismatch can result in increased expression ofthe KIT oncogene. genetics_GWAS hsa-mir-25 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-296 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-302a Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-302b Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-302c Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-302d Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-30b Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-30d Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-320a Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-338 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-339 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-367 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-383 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number loss genetics_GWAS hsa-mir-429 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-488 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-9-1 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-93 Melanoma 16754881 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 copy number gain genetics_GWAS hsa-mir-124 Mesial Temporal Lobe Epilepsy 27188998 G40.209 D004833 608096 In this study, the effect of the SNP of one neuronal miRNA, miR-124, on susceptibility to MTLE was investigated using a case control study. genetics_GWAS hsa-mir-146a Metabolic Syndrome 25958310 disease of metabolism DOID:14221 E88.81 D024821 605552 The C allele of miRNA-146a rs2910164 showed positive association with increased susceptibility to metabolic syndrome and its phenotypes in the study population. genetics_GWAS hsa-mir-146a Moyamoya Disease 22659075 cardiovascular system disease DOID:13099 I67.5 D009072 PS252350 HP:0011834 Association of the miR-146aC>G, miR-196a2C>T, and miR-499A>G polymorphisms with moyamoya disease in the Korean population. genetics_GWAS hsa-mir-196a-2 Moyamoya Disease 22659075 cardiovascular system disease DOID:13099 I67.5 D009072 PS252350 HP:0011834 Association of the miR-146aC>G, miR-196a2C>T, and miR-499A>G polymorphisms with moyamoya disease in the Korean population. genetics_GWAS hsa-mir-15a Multiple Myeloma 20031211 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 miR-15a:Micro-RNA-15a and micro-RNA-16 expression and chromosome 13 deletions in multiple myeloma genetics_GWAS hsa-mir-16-1 Multiple Myeloma 20031211 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 miR-16:Micro-RNA-15a and micro-RNA-16 expression and chromosome 13 deletions in multiple myeloma genetics_GWAS hsa-mir-16-2 Multiple Myeloma 20031211 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 miR-16:Micro-RNA-15a and micro-RNA-16 expression and chromosome 13 deletions in multiple myeloma genetics_GWAS hsa-mir-146a Multiple Sclerosis 25591770 nervous system disease DOID:2377 G35 D009103 PS126200 rs2910164 may play a role in MS susceptibility in females. The rs2910164 G>C variation may affect the expression of miR-146a and the release of proinflammatory cytokines. genetics_GWAS hsa-mir-2278 Multiple Sclerosis 24638856 nervous system disease DOID:2377 G35 D009103 PS126200 Assessment of microRNA-related SNP effects in the 3' untranslated region of the IL22RA2 risk locus in multiple sclerosis. genetics_GWAS hsa-mir-411 Multiple Sclerosis 24638856 nervous system disease DOID:2377 G35 D009103 PS126200 Assessment of microRNA-related SNP effects in the 3' untranslated region of the IL22RA2 risk locus in multiple sclerosis. genetics_GWAS hsa-mir-548ac Multiple Sclerosis 25795118 nervous system disease DOID:2377 G35 D009103 PS126200 Susceptibility variants in the CD58 gene locus point to a role of microRNA-548ac in the pathogenesis of multiple sclerosis. genetics_GWAS hsa-mir-424 Myelodysplastic Syndromes 24674452 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 Detection of an activated JAK3 variant and a Xq26.3 microdeletion causing loss of PHF6 and miR-424 expression in myelodysplastic syndromes by combined targeted next generation sequencing and SNP array analysis. genetics_GWAS hsa-mir-126 Myocardial Infarction 29304813 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 The association between pre-miR-27a rs895819 polymorphism and myocardial infarction risk in a Chinese Han population genetics_GWAS hsa-mir-146a Myocardial Infarction 24850191 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Association of microRNA polymorphisms with the risk of myocardial infarction in a Chinese population. genetics_GWAS hsa-mir-149 Myocardial Infarction 24850191 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Association of microRNA polymorphisms with the risk of myocardial infarction in a Chinese population. genetics_GWAS hsa-mir-196a-2 Myocardial Infarction 24850191 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Association of microRNA polymorphisms with the risk of myocardial infarction in a Chinese population. genetics_GWAS hsa-mir-218 Myocardial Infarction 24850191 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Association of microRNA polymorphisms with the risk of myocardial infarction in a Chinese population. genetics_GWAS hsa-mir-499 Myocardial Infarction 24850191 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Association of microRNA polymorphisms with the risk of myocardial infarction in a Chinese population. genetics_GWAS hsa-mir-328 Myopia 21421876 nervous system disease DOID:11830 H52.1 D009216 PS160700 SNPs rs644242 and rs662702 had marginal significance (p=0.063) and further analyses showed that these SNPs were associated with extreme myopia. The OR for extreme myopia was 2.1 (empirical p=0.007) for the CC genotype at SNP rs662702 at 3' UTR. The functional assay for SNP rs662702 demonstrated that the C allele had a significantly lower expression level than the T allele (P=0.0001). SNP rs662702 was predicted to be located in the microRNA-328 binding site, which may explain the differential allelic effect on gene expression. genetics_GWAS hsa-mir-146a Nasopharyngeal Neoplasms 22711332 C11.9 D009303 607107 HP:0100630 A single nucleotide polymorphism (rs2910164) in microRNA-146a is associated with the risk for nasopharyngeal carcinoma. genetics_GWAS hsa-mir-151a Nasopharyngeal Neoplasms 23416081 C11.9 D009303 607107 HP:0100630 A miR-151 binding site polymorphism in the 3'-untranslated region of the cyclin E1 gene associated with nasopharyngeal carcinoma genetics_GWAS hsa-mir-151b Nasopharyngeal Neoplasms 23416081 C11.9 D009303 607107 HP:0100630 A miR-151 binding site polymorphism in the 3'-untranslated region of the cyclin E1 gene associated with nasopharyngeal carcinoma genetics_GWAS hsa-mir-34b Nasopharyngeal Neoplasms 23504554 C11.9 D009303 607107 HP:0100630 Interactions of miR-34b/c and TP-53 polymorphisms on the risk of nasopharyngeal carcinoma genetics_GWAS hsa-mir-34c Nasopharyngeal Neoplasms 23504554 C11.9 D009303 607107 HP:0100630 Interactions of miR-34b/c and TP-53 polymorphisms on the risk of nasopharyngeal carcinoma genetics_GWAS hsa-mir-124 Neoplasms [unspecific] 26625819 C80.1 D009369 This meta-analysis suggests that the miR-124 rs531564 C > G polymorphism is an important risk factor for cancers among the Chinese population. genetics_GWAS hsa-mir-146a Neoplasms [unspecific] 24278149 C80.1 D009369 Association between microRNA polymorphisms and cancer risk based on the findings of 66 case-control studies. genetics_GWAS hsa-mir-146a Neoplasms [unspecific] 24716941 C80.1 D009369 Association analysis of single nucleotide polymorphisms in miR-146a and miR-196a2 on the prevalence of cancer in elderly Japanese: a case-control study. genetics_GWAS hsa-mir-146a Neoplasms [unspecific] 26337564 C80.1 D009369 We conclude that rs2910164 may represent a valuable biomarker associated with the risk of developing specific types of cancer. genetics_GWAS hsa-mir-149 Neoplasms [unspecific] 24278149 C80.1 D009369 Association between microRNA polymorphisms and cancer risk based on the findings of 66 case-control studies. genetics_GWAS hsa-mir-155 Neoplasms [unspecific] 27531892 C80.1 D009369 Our findings suggested that miR-155 and its functional variant rs767649 might contribute to the increased risk and poor prognosis of HCC genetics_GWAS hsa-mir-196a Neoplasms [unspecific] 23691458 C80.1 D009369 The meta-analysis demonstrated that the miR-196a-2 polymorphism is associated with cancer susceptibility, especially lung cancer, colorectal cancer, and breast cancer among Asian populations. genetics_GWAS hsa-mir-196a-2 Neoplasms [unspecific] 24278149 C80.1 D009369 Association between microRNA polymorphisms and cancer risk based on the findings of 66 case-control studies. genetics_GWAS hsa-mir-196a-2 Neoplasms [unspecific] 24716941 C80.1 D009369 Association analysis of single nucleotide polymorphisms in miR-146a and miR-196a2 on the prevalence of cancer in elderly Japanese: a case-control study. genetics_GWAS hsa-mir-204 Neoplasms [unspecific] 20439436 C80.1 D009369 miR-204:hsa-miR-30 and hsa-miR-204, were found to be physically altered at the DNA copy number level as well genetics_GWAS hsa-mir-20a Neoplasms [unspecific] 20439436 C80.1 D009369 mir-20a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_GWAS hsa-mir-218 Neoplasms [unspecific] 24761857 C80.1 D009369 The findings suggest that pre-miR-218 rs11134527 polymorphism may have some relation to cancer development in Chinese. However, well-designed studies with larger sample size and more detailed data are needed to confirm these conclusions. genetics_GWAS hsa-mir-30a Neoplasms [unspecific] 20439436 C80.1 D009369 miR-30:hsa-miR-103/106 were downgraded in cancer, whereas hsa-miR-30 became most prominent genetics_GWAS hsa-mir-34b Neoplasms [unspecific] 25190019 C80.1 D009369 The genetic association between pri-miR-34b/c polymorphism (rs4938723 T>C) and susceptibility to cancers: evidence from published studies. genetics_GWAS hsa-mir-34c Neoplasms [unspecific] 25190019 C80.1 D009369 The genetic association between pri-miR-34b/c polymorphism (rs4938723 T>C) and susceptibility to cancers: evidence from published studies. genetics_GWAS hsa-mir-423 Neoplasms [unspecific] 28430524 C80.1 D009369 miRNA-Related Polymorphisms in miR-423 (rs6505162) and PEX6 (rs1129186) and Risk of Esophageal Squamous Cell Carcinoma in an Iranian Cohort. genetics_GWAS hsa-mir-499 Neoplasms [unspecific] 24085457 C80.1 D009369 The miR-499 rs3746444 polymorphism is associated with an increased cancer risk. genetics_GWAS hsa-mir-499 Neoplasms [unspecific] 24278149 C80.1 D009369 Association between microRNA polymorphisms and cancer risk based on the findings of 66 case-control studies. genetics_GWAS hsa-mir-499 Neoplasms [unspecific] 25433484 C80.1 D009369 hsa-mir-499 rs3746444 T > C polymorphism is associated with the risk of cancer in Asians, mainly in Iranian and Chinese population. However, rs3746444 T > C polymorphism is negatively associated with the risk of esophageal cancer. genetics_GWAS hsa-mir-499 Neoplasms [unspecific] 25640376 C80.1 D009369 hsa-mir-499 rs3746444 A>G polymorphism is not associated with risk of cancer based on current evidence. genetics_GWAS hsa-mir-499 Neoplasms [unspecific] 24258110 C80.1 D009369 Quantitative assessment of the association between microRNA-499 rs3746444 A/G polymorphism and cancer risk. genetics_GWAS hsa-mir-34a Neuroblastoma 27805929 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Genetic variant rs3750625 in the 3'UTR of ADRA2A affects stress-dependent acute pain severity after trauma and alters a microRNA-34a regulatory site. genetics_GWAS hsa-mir-26a Neurodegenerative Diseases [unspecific] 25074322 D019636 HP:0002180 A functional SNP catalog of overlapping miRNA-binding sites in genes implicated in prion disease and other neurodegenerative disorders. genetics_GWAS hsa-mir-181a Neuroinflammation 28769921 MicroRNA-181 Variants Regulate T Cell Phenotype in the Context of Autoimmune Neuroinflammation genetics_GWAS hsa-mir-181b Neuroinflammation 28769921 MicroRNA-181 Variants Regulate T Cell Phenotype in the Context of Autoimmune Neuroinflammation. genetics_GWAS hsa-mir-124-1 Neuropsychiatric Disorders [unspecific] 25841663 C537163 We showed for the first time the association of a functional polymorphism in MIR124-1 and aggressiveness. Known targets of miR-124 (such as BDNF and DRD4 genes) could explain the effect of this miRNA on behavior. A future analysis of additional novel functional polymorphisms in other brain expressed miRNAs could be useful for a deeper understanding of aggression in humans. genetics_GWAS hsa-mir-365 Neuropsychiatric Disorders [unspecific] 27074815 C537163 single nucleotide polymorphism (SNP) rs2235749 (in high linkage disequilibrium with rs910080) modifies striatal PDYN expression via impaired binding of miR-365 genetics_GWAS hsa-mir-3649 Non-Syndromic Orofacial Clefts 24603642 PS119530 Taken together, these findings indicate that SNPs in the miRNA-binding sites might play an important role in the development of NSOCs. Furthermore, if confirmed in subsequent studies, the polymorphisms may be considered as additional markers for the evaluation of infants' risk of NSOCs. genetics_GWAS hsa-mir-26b Obesity 24807789 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 Expression of microRNA-26b, an obesity-related microRNA, is regulated by free fatty acids, glucose, dexamethasone and growth hormone in human adipocytes. genetics_GWAS hsa-mir-27a Obesity 27537871 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 MicroRNAs and Drinking: Association between the Pre-miR-27a rs895819 Polymorphism and Alcohol Consumption in a Mediterranean Population. genetics_GWAS hsa-mir-122 Oral Neoplasms 25981582 C06.9 D009062 HP:0100649 These results suggest that IL-1α 3' UTR rs3783553 polymorphism may be functional and influence susceptibility to HPV16-associated OSCC, particularly for SCCOP. Validation of our findings is warranted. genetics_GWAS hsa-mir-29a Oral Neoplasms 24885463 C06.9 D009062 HP:0100649 Variations in microRNAs and their processing genes modulated risk of precancer but further in-depth study is needed to understand mechanism of disease process. genetics_GWAS hsa-mir-34b Oral Neoplasms 24297336 C06.9 D009062 HP:0100649 Genetic variations at microRNA and processing genes and risk of oral cancer. genetics_GWAS hsa-mir-34b Oral Neoplasms 24885463 C06.9 D009062 HP:0100649 Variations in microRNAs and their processing genes modulated risk of precancer but further in-depth study is needed to understand mechanism of disease process. genetics_GWAS hsa-mir-423 Oral Neoplasms 24885463 C06.9 D009062 HP:0100649 Variations in microRNAs and their processing genes modulated risk of precancer but further in-depth study is needed to understand mechanism of disease process. genetics_GWAS hsa-mir-146a Ossification of Posterior Longitudinal Ligament 27454313 musculoskeletal system disease DOID:0060887 M48.8 D017887 602475 The miR-146a/-149/-196a2/-499 allele combinations may be a genetic risk factor for cervical OPLL in the Korean population. genetics_GWAS hsa-mir-149 Ossification of Posterior Longitudinal Ligament 27454313 musculoskeletal system disease DOID:0060887 M48.8 D017887 602475 The miR-146a/-149/-196a2/-499 allele combinations may be a genetic risk factor for cervical OPLL in the Korean population. genetics_GWAS hsa-mir-196a2 Ossification of Posterior Longitudinal Ligament 27454313 musculoskeletal system disease DOID:0060887 M48.8 D017887 602475 The miR-146a/-149/-196a2/-499 allele combinations may be a genetic risk factor for cervical OPLL in the Korean population. genetics_GWAS hsa-mir-499 Ossification of Posterior Longitudinal Ligament 27454313 musculoskeletal system disease DOID:0060887 M48.8 D017887 602475 The results indicate that GG genotype of miR-499 is associated with significantly higher risks of OPLL in the segmental OPLL group. genetics_GWAS hsa-mir-34b Osteoporosis 27227383 musculoskeletal system disease DOID:11476 M80 D010024 166710 HP:0000939 The present findings indicate that pri-miR-34b/c rs4938723 and TP53 Arg72Pro polymorphisms may contribute to the risk of OP. genetics_GWAS hsa-mir-34c Osteoporosis 27227383 musculoskeletal system disease DOID:11476 M80 D010024 166710 HP:0000939 The present findings indicate that pri-miR-34b/c rs4938723 and TP53 Arg72Pro polymorphisms may contribute to the risk of OP. genetics_GWAS hsa-mir-98 Osteoporosis 29307778 musculoskeletal system disease DOID:11476 M80 D010024 166710 HP:0000939 Computational and functional characterization of four SNPs in the SOST locus associated with osteoporosis genetics_GWAS hsa-let-7a Osteosarcoma 27430246 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Taken together, the findings of the present study demonstrated that the KRAS 3'-UTR rs61764370 polymorphism interfered with miRNA/mRNA interaction, and showed that the minor allele was associated with an elevated risk of developing metastatic disease in OS. genetics_GWAS hsa-mir-124a Osteosarcoma 27540978 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Single nucleotide polymorphism of hsa-miR-124a affects risk and prognosis of osteosarcoma. genetics_GWAS hsa-mir-17 Osteosarcoma 25663449 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 This study suggests that SNPs in RISC complex genes may be involved in osteosarcoma susceptibility, especially rs11866002 in CNOT1. genetics_GWAS hsa-mir-18 Osteosarcoma 25663449 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 This study suggests that SNPs in RISC complex genes may be involved in osteosarcoma susceptibility, especially rs11866002 in CNOT1. genetics_GWAS hsa-mir-19a Osteosarcoma 25663449 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 This study suggests that SNPs in RISC complex genes may be involved in osteosarcoma susceptibility, especially rs11866002 in CNOT1. genetics_GWAS hsa-mir-19b-1 Osteosarcoma 25663449 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 This study suggests that SNPs in RISC complex genes may be involved in osteosarcoma susceptibility, especially rs11866002 in CNOT1. genetics_GWAS hsa-mir-20a Osteosarcoma 25663449 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 This study suggests that SNPs in RISC complex genes may be involved in osteosarcoma susceptibility, especially rs11866002 in CNOT1. genetics_GWAS hsa-mir-92-1 Osteosarcoma 25663449 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 This study suggests that SNPs in RISC complex genes may be involved in osteosarcoma susceptibility, especially rs11866002 in CNOT1. genetics_GWAS hsa-let-7a-1 Ovarian Neoplasms 21482675 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 rs12194974 (G>A), a SNP in a putative transcription factor binding site in the LIN28B promoter region (summary OR=0.90, 95% CI: 0.82-0.98; P=0.015). LIN28B LIN28B over-expression in epithelial ovarian cancer (EOC) contributes to tumorigenesis by repressing tumor suppressor let-7 expression. genetics_GWAS hsa-let-7a-2 Ovarian Neoplasms 21482675 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 rs12194974 (G>A), a SNP in a putative transcription factor binding site in the LIN28B promoter region (summary OR=0.90, 95% CI: 0.82-0.98; P=0.015). LIN28B LIN28B over-expression in epithelial ovarian cancer (EOC) contributes to tumorigenesis by repressing tumor suppressor let-7 expression. genetics_GWAS hsa-let-7a-2 Ovarian Neoplasms 22970210 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 We found that there was a reduction in the copy number of let-7 genes in a cancer-type specific manner. Importantly, focal deletion of four let-7 family members was found in three cancer types: medulloblastoma (let-7a-2 and let-7e), breast cancer (let-7a-2), and ovarian cancer (let-7a-3/let-7b). genetics_GWAS hsa-let-7a-3 Ovarian Neoplasms 21482675 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 rs12194974 (G>A), a SNP in a putative transcription factor binding site in the LIN28B promoter region (summary OR=0.90, 95% CI: 0.82-0.98; P=0.015). LIN28B LIN28B over-expression in epithelial ovarian cancer (EOC) contributes to tumorigenesis by repressing tumor suppressor let-7 expression. genetics_GWAS hsa-let-7e Ovarian Neoplasms 22970210 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 We found that there was a reduction in the copy number of let-7 genes in a cancer-type specific manner. Importantly, focal deletion of four let-7 family members was found in three cancer types: medulloblastoma (let-7a-2 and let-7e), breast cancer (let-7a-2), and ovarian cancer (let-7a-3/let-7b). genetics_GWAS hsa-mir-103a-2 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-106b Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-1-1 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-133a-2 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-135b Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-146a Ovarian Neoplasms 18660546 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 miR-146a: A functional polymorphism (rs2910164) in the miR-146a gene and age of familial breast/ovarian cancer diagnosis genetics_GWAS hsa-mir-146a Ovarian Neoplasms 26785832 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 e identified one rare variant in MIR146A, four in MIR146B, five in BRCA1 3'-UTR and one in BRCA2 3'-UTR in 716 index cases and 619 controls. genetics_GWAS hsa-mir-146b Ovarian Neoplasms 26785832 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 we identified one rare variant in MIR146A, four in MIR146B, five in BRCA1 3'-UTR and one in BRCA2 3'-UTR in 716 index cases and 619 controls. genetics_GWAS hsa-mir-151a Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-153-2 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-17 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-17 Ovarian Neoplasms 22235027 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113 genetics_GWAS hsa-mir-18a Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-18a Ovarian Neoplasms 22235027 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113 genetics_GWAS hsa-mir-191 Ovarian Neoplasms 20167074 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Novel genetic variants in miR-191 gene and familial ovarian cancer genetics_GWAS hsa-mir-194-1 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-199a-2 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-19a Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-19a Ovarian Neoplasms 22235027 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113 genetics_GWAS hsa-mir-19b-1 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-19b-1 Ovarian Neoplasms 22235027 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113 genetics_GWAS hsa-mir-200a Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-200b Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-20a Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-20a Ovarian Neoplasms 22235027 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113 genetics_GWAS hsa-mir-214 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-215 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-218-1 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-219-1 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-25 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-296 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-302a Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-302b Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-302c Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-302d Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-30b Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-30d Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-320a Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-338 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-339 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-367 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-383 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number loss genetics_GWAS hsa-mir-429 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-488 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-502 Ovarian Neoplasms 22867998 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 A polymorphism (rs16917496) at the miR-502 binding site in the 3' untranslated region of the SET8 gene is associated with the risk of epithelial ovarian cancer. genetics_GWAS hsa-mir-9-1 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-92a-1 Ovarian Neoplasms 22235027 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113 genetics_GWAS hsa-mir-93 Ovarian Neoplasms 16754881 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 copy number gain genetics_GWAS hsa-mir-34a Parkinson Disease 25541488 nervous system disease DOID:14330 G20 D010300 PS168600 down-regulation of miR-34b and miR-34c in the brain, as well as an SNP in the 3'-UTR of α-syn can increase α-syn expression, possibly contributing to PD pathogenesis. genetics_GWAS hsa-mir-584 Pemphigus 27424220 integumentary system disease DOID:9182 L10 D010392 Collectively, these results suggest that a disease-associated SNP located within the 3'UTR of KLRG1 directly interferes with miR-584-5p binding, allowing for KLRG1 mRNA differential accumulation, which in turn may contribute to pathogenesis of autoimmune diseases, such as pemphigus. genetics_GWAS hsa-mir-611 Pleural Mesothelioma 25436799 disease of cellular proliferation DOID:7474 C45.0 D054363 HP:0100002 MRP performance as diagnostic biomarker improved by considering the genotype rs1057147. This polymorphism most likely affects a binding site for miR-611. genetics_GWAS hsa-mir-146a Polycystic Ovarian Syndrome 29637801 syndrome DOID:11612 E28.2 D011085 184700 women with miR-146a variation are at a higher risk for developing PCOS, which can be due to up-regulation of miR-146a genetics_GWAS hsa-mir-518 Premature Ovarian Failure 25365407 endocrine system disease DOID:5426 E28.3 D016649 PS311360 Association study of TGFBR2 and miR-518 gene polymorphisms with age at natural menopause, premature ovarian failure, and early menopause among Chinese Hanwomen. genetics_GWAS hsa-mir-125b-1 Prostate Neoplasms 21556765 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 rs1434536 in the 3'UTR of BMPR1B gene affects the binding ability of miR-125b to BMPR1B mRNA and contributes to the genetic hspredisposition to localized prostate cancer and patients aged >70years. genetics_GWAS hsa-mir-125b-2 Prostate Neoplasms 21556765 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 rs1434536 in the 3'UTR of BMPR1B gene affects the binding ability of miR-125b to BMPR1B mRNA and contributes to the genetic hspredisposition to localized prostate cancer and patients aged >70years. genetics_GWAS hsa-mir-143 Prostate Neoplasms 25354797 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 there is the significant association between the functional promoter variant rs4705342T>C in miR-143 and PCa risk genetics_GWAS hsa-mir-146a Prostate Neoplasms 25084752 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Association between genetic variant in hsa-miR-146a gene and prostate cancer progression genetics_GWAS hsa-mir-146a Prostate Neoplasms 19902466 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The natural genetic variation in pre-miR-146a affects the amount of mature miR-146a, contributes to the genetic predisposition to CaP. genetics_GWAS hsa-mir-196a-2 Prostate Neoplasms 26112096 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Assessment of association between genetic variants in microRNA genes hsa-miR-499,hsa-miR-196a2 and hsa-miR-27a and prostate cancer risk in Serbian population. genetics_GWAS hsa-mir-27a Prostate Neoplasms 26112096 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Assessment of association between genetic variants in microRNA genes hsa-miR-499,hsa-miR-196a2 and hsa-miR-27a and prostate cancer risk in Serbian population. genetics_GWAS hsa-mir-3162 Prostate Neoplasms 25691096 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Findings from this large association study suggest that a focus on miRSNPs, including functional evaluation, can identify candidate risk loci below currently accepted statistical levels of genome-wide significance. Studies of miRNAs and their interactions with SNPs could provide further insights into the mechanisms of prostate cancer risk. genetics_GWAS hsa-mir-370 Prostate Neoplasms 25691096 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Findings from this large association study suggest that a focus on miRSNPs, including functional evaluation, can identify candidate risk loci below currently accepted statistical levels of genome-wide significance. Studies of miRNAs and their interactions with SNPs could provide further insights into the mechanisms of prostate cancer risk. genetics_GWAS hsa-mir-499 Prostate Neoplasms 26112096 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Assessment of association between genetic variants in microRNA genes hsa-miR-499,hsa-miR-196a2 and hsa-miR-27a and prostate cancer risk in Serbian population. genetics_GWAS hsa-mir-146a Psoriasis 25209759 integumentary system disease DOID:8893 L40.9 D011565 PS177900 HP:0003765 A single-nucleotide polymorphism of miR-146a and psoriasis: an association and functional study. genetics_GWAS hsa-mir-146a Psoriasis 27098222 integumentary system disease DOID:8893 L40.9 D011565 PS177900 HP:0003765 The miR-146a SNPs rs2910164, rs57095329, rs2431697 are associated with susceptibility to certain autoimmune diseases. genetics_GWAS hsa-mir-146a Psoriasis 29587639 integumentary system disease DOID:8893 L40.9 D011565 PS177900 HP:0003765 A single nucleotide polymorphism in the miR-146a gene (rs2910164), aberrantly alters its gene expression and linked with the pathogenesis of several disorders, including psoriasis and PsA genetics_GWAS hsa-mir-492 Psoriasis 21655935 integumentary system disease DOID:8893 L40.9 D011565 PS177900 HP:0003765 The rs8259 T allele was associated with significantly decreased psoriasis susceptibility (OR=0.758, 95% CI 0.638-0.901, p=0.002) compared to A allele. the rs8259 polymorphism was located in a seed region for miR-492 binding. genetics_GWAS hsa-mir-146a Psoriatic Arthritis 29587639 syndrome DOID:9008 L40.5 D015535 607507 A single nucleotide polymorphism in the miR-146a gene (rs2910164), aberrantly alters its gene expression and linked with the pathogenesis of several disorders, including psoriasis and PsA genetics_GWAS hsa-mir-137 Psychiatric Disorders 23786914 D001523 604363 Analysis of miR-137 expression and rs1625579 in dorsolateral prefrontal cortex. genetics_GWAS hsa-mir-146b Psychiatric Disorders 25771167 D001523 604363 Our findings highlight trans effects of common variants on microRNA-mediated gene expression as an integral part of the genetic architecture of complex disorders and traits. genetics_GWAS hsa-mir-330 Psychiatric Disorders 24436253 D001523 604363 The effects of a MAP2K5 microRNA target site SNP on risk for anxiety and depressive disorders. genetics_GWAS hsa-mir-146a Pulmonary Hypertension 26202355 cardiovascular system disease DOID:6432 I27.20 D006976 PS178600 HP:0002092 the results of this study demonstrate that the rs2910164 CC and GC genotype is associated with a decreased risk of pulmonary hypertension, which could be attributed to defective miRNA processing and compromised ability to inhibit production of COX-2 and PGI2. genetics_GWAS hsa-mir-608 Rectal Neoplasms 27381831 disease of cellular proliferation DOID:1984 D012004 Sequence variation in mature microRNA-608 and benefit from neo-adjuvant treatment in locally advanced rectal cancer patients. genetics_GWAS hsa-mir-34b Retinoblastoma 28106538 nervous system disease DOID:768 C69.20 D012175 180200 HP:0009919 A polymorphism in mir-34b/c as a potential biomarker for early onset of hereditary retinoblastoma. genetics_GWAS hsa-mir-34c Retinoblastoma 28106538 nervous system disease DOID:768 C69.20 D012175 180200 HP:0009919 A polymorphism in mir-34b/c as a potential biomarker for early onset of hereditary retinoblastoma. genetics_GWAS hsa-mir-146a Rheumatoid Arthritis 24824381 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Association of two polymorphisms rs2910164 in miRNA-146a and rs3746444 in miRNA-499 with rheumatoid arthritis: a meta-analysis. genetics_GWAS hsa-mir-146a Rheumatoid Arthritis 27342690 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 12 single nucleotide polymorphisms genetics_GWAS hsa-mir-146a Rheumatoid Arthritis 28083614 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Significance of Polymorphism and Expression of miR-146a and NFkB1 Genetic Variants in Patients with Rheumatoid Arthritis. genetics_GWAS hsa-mir-149 Rheumatoid Arthritis 26032077 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 SNP rs22928323 in miR-149 is correlated with RA in the east of Chinese Han population, whereas there is no correlation between miR-149 polymorphism and clinical characteristics in patients with RA. genetics_GWAS hsa-mir-499 Rheumatoid Arthritis 24327058 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 This study suggested that miR-499 polymorphisms were associated with a significantly increased risk of RA in Mediterranean populations. genetics_GWAS hsa-mir-499 Rheumatoid Arthritis 24824381 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Association of two polymorphisms rs2910164 in miRNA-146a and rs3746444 in miRNA-499 with rheumatoid arthritis: a meta-analysis. genetics_GWAS hsa-mir-499a Rheumatoid Arthritis 22019503 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 There was a significant difference in the levels of CRP and ESR among different genotypes in rs3746444 (hsa-mir-499) (p = 0.031 and p = 0.047, respectively) in Chinese Han people. The heterozygote CT had significantly higher levels of CRP and ESR compared with homozygotes CC and TT. genetics_GWAS hsa-mir-137 Schizophrenia 25044277 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 The miR-137 schizophrenia susceptibility variant rs1625579 does not predict variability in brain volume in a sample of schizophrenic patients and healthy individuals. genetics_GWAS hsa-mir-137 Schizophrenia 21926974 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 GWAS analysis revealed that rs1625579 within an intron of a putative primary transcript for MIR137 (microRNA 137), a known regulator of neuronal development was associated with schizophrenia. genetics_GWAS hsa-mir-137 Schizophrenia 24132022 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 Impact of the genome-wide schizophrenia risk single nucleotide polymorphism (rs1625579) in miR-137 on brain structures in healthy individuals. genetics_GWAS hsa-mir-137 Schizophrenia 25921703 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 The impact of genome wide supported microRNA-137 (MIR137) risk variants on frontal and striatal white matter integrity, neurocognitive functioning, and negative symptoms in schizophrenia. genetics_GWAS hsa-mir-137 Schizophrenia 26836412 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 Polymorphisms in MIR137HG and microRNA-137-regulated genes influence gray matter structure in schizophrenia. genetics_GWAS hsa-mir-137 Schizophrenia 25241074 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 Lack of association between microRNA-137 SNP rs1625579 and schizophrenia in a replication study of Han Chinese. genetics_GWAS hsa-mir-137 Schizophrenia 25434007 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 rare noncoding risk variants are associated with SZ and BP at MIR137/MIR2682 locus, with risk alleles decreasing MIR137/MIR2682 expression. genetics_GWAS hsa-mir-137 Schizophrenia 26429811 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 A GWAS SNP for Schizophrenia Is Linked to the Internal MIR137 Promoter and Supports Differential Allele-Specific Expression. genetics_GWAS hsa-mir-137 Schizophrenia 27096222 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 A single nucleotide polymorphism rs1625579 in the miR-137 gene has recently been reported to confer risk of schizophrenia genetics_GWAS hsa-mir-137 Schizophrenia 27525637 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 Genome-wide association studies (GWAS) have identified a region at chromosome 1p21.3, containing the microRNA MIR137, to be among the most significant associations for schizophrenia. genetics_GWAS hsa-mir-198 Schizophrenia 17849003 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 SNP (rs1700) disease susceptibility genetics_GWAS hsa-mir-206 Schizophrenia 17849003 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 SNP (rs17578796) disease susceptibility genetics_GWAS hsa-mir-206 Schizophrenia 27424800 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 Our study therefore suggests that miR-206 may contribute to schizophrenia risk through allele-dependent regulation of the genome-wide significant gene NT5C2. genetics_GWAS hsa-mir-219 Schizophrenia 26257337 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 These findings suggest that GRIN2B may be associated with schizophrenia and interaction effects of the polymorphisms in hsa-miR-219, CAKM2G, GRIN2B and GRIN3A may confer susceptibility to schizophrenia in the Chinese Han population. genetics_GWAS hsa-mir-2682 Schizophrenia 25434007 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 rare noncoding risk variants are associated with SZ and BP at MIR137/MIR2682 locus, with risk alleles decreasing MIR137/MIR2682 expression. genetics_GWAS hsa-mir-30e Schizophrenia 20347265 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 miR-30e:mir-30e ss178077483 plays a role in schizophrenia susceptibility genetics_GWAS hsa-mir-30e Schizophrenia 20579744 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 Our previous study revealed a strong association between the polymorphism ss178077483 in the miRNA-30e precursor (pre-miR-30e) and the risk of SCZ. genetics_GWAS hsa-mir-96 Sensorineural Hearing Loss 19363478 nervous system disease DOID:10003 H90.5 D006313 304400 miR-96: An ENU-induced mutation genetics_GWAS hsa-mir-96 Sensorineural Hearing Loss 19363479 nervous system disease DOID:10003 H90.5 D006313 304400 miR-96: Mutations in the seed region genetics_GWAS hsa-mir-146a Sepsis 24701036 A41.9 D018805 HP:0100806 The functional polymorphisms of miR-146a are associated with susceptibility to severe sepsis in the Chinese population. genetics_GWAS hsa-mir-146a Skin Neoplasms 24699816 disease of cellular proliferation DOID:4159 C44.90 D012878 HP:0008069 we investigated the impact of MIR146A SNP rs2910164 on cancer risk, and interaction with a SNP in one of its putative targets (RNASEL, rs486907). genetics_GWAS hsa-mir-149 Squamous Cell Carcinoma 27050146 disease of cellular proliferation DOID:1749 D002294 hsa-mir-149 rs2292832 and hsa-mir-499 rs3746444 polymorphisms play a significant role in the prognosis of SCCNOP genetics_GWAS hsa-let-7i Squamous Cell Carcinoma, Cerevial 29154871 endocrine system disease DOID:5531 Association between genetic polymorphisms in the promoters of let-7 and risk of cervical squamous cell carcinoma genetics_GWAS hsa-mir-122 Squamous Cell Carcinoma, Cerevial 25955681 endocrine system disease DOID:5531 These findings indicate that the IL1A rs3783553 polymorphism may be associated with the etiology of CSCC. genetics_GWAS hsa-mir-146a Squamous Cell Carcinoma, Cerevial 21319225 endocrine system disease DOID:5531 SNP (rs2910164 G/C): Significantly increased CSCC risks were found to be associated with G allele of rs2910164 genetics_GWAS hsa-mir-499a Squamous Cell Carcinoma, Cerevial 21319225 endocrine system disease DOID:5531 SNP (rs3746444 A/G): Significantly increased CSCC risks were found to be associated with G allele of rs3746444 genetics_GWAS hsa-mir-100 Squamous Cell Carcinoma, Esophageal 26261633 disease of cellular proliferation DOID:3748 C562729 Genetic variation in miR-100 rs1834306 is associated with decreased risk for esophageal squamous cell carcinoma in Kazakh patients in northwest China. genetics_GWAS hsa-mir-100 Squamous Cell Carcinoma, Esophageal 24288122 disease of cellular proliferation DOID:3748 C562729 Taken together, these findings indicate that miRNA polymorphisms may predict prognosis in advanced ESCC patients receiving platinum-based chemotherapy. genetics_GWAS hsa-mir-124 Squamous Cell Carcinoma, Esophageal 24945256 disease of cellular proliferation DOID:3748 C562729 Pri-miR-124 rs531564 and pri-miR-34b/c rs4938723 polymorphisms are associated with decreased risk of esophageal squamous cell carcinoma in Chinese populations. genetics_GWAS hsa-mir-125a Squamous Cell Carcinoma, Esophageal 24288122 disease of cellular proliferation DOID:3748 C562729 Taken together, these findings indicate that miRNA polymorphisms may predict prognosis in advanced ESCC patients receiving platinum-based chemotherapy. genetics_GWAS hsa-mir-146a Squamous Cell Carcinoma, Esophageal 23792053 disease of cellular proliferation DOID:3748 C562729 These findings indicated that functional polymorphism miR-196a2 rs11614913 T > C might contribute to decreased ESCC risk among women patients and patients who never smoking or drinking. However, our results were obtained with a limited sample size. Future larger studies with other ethnic populations and tissue-specific biological characterization are required to confirm current findings. genetics_GWAS hsa-mir-146a Squamous Cell Carcinoma, Esophageal 24288122 disease of cellular proliferation DOID:3748 C562729 Taken together, these findings indicate that miRNA polymorphisms may predict prognosis in advanced ESCC patients receiving platinum-based chemotherapy. genetics_GWAS hsa-mir-184 Squamous Cell Carcinoma, Esophageal 25383966 disease of cellular proliferation DOID:3748 C562729 Our data demonstrate that functional TNFAIP2 rs8126 genetic variant is a ESCC susceptibility SNP. genetics_GWAS hsa-mir-196a-2 Squamous Cell Carcinoma, Esophageal 24320161 disease of cellular proliferation DOID:3748 C562729 These results suggest that the miRNA-196a2 functional polymorphism rs11614913 might be an effective genetic marker for ESCC risk assessment in individuals younger than 60 years of age from a region of high ESCC incidence in northern China. genetics_GWAS hsa-mir-196a-2 Squamous Cell Carcinoma, Esophageal 24288122 disease of cellular proliferation DOID:3748 C562729 Taken together, these findings indicate that miRNA polymorphisms may predict prognosis in advanced ESCC patients receiving platinum-based chemotherapy. genetics_GWAS hsa-mir-196a-2 Squamous Cell Carcinoma, Esophageal 23792053 disease of cellular proliferation DOID:3748 C562729 These findings indicated that functional polymorphism miR-196a2 rs11614913 T > C might contribute to decreased ESCC risk among women patients and patients who never smoking or drinking. However, our results were obtained with a limited sample size. Future larger studies with other ethnic populations and tissue-specific biological characterization are required to confirm current findings. genetics_GWAS hsa-mir-214 Squamous Cell Carcinoma, Esophageal 27323028 disease of cellular proliferation DOID:3748 C562729 esophageal squamous cell carcinoma genetics_GWAS hsa-mir-218 Squamous Cell Carcinoma, Esophageal 25337271 disease of cellular proliferation DOID:3748 C562729 The impact of pri-miR-218 rs11134527 on the risk and prognosis of patients with esophageal squamous cell carcinoma. genetics_GWAS hsa-mir-219-1 Squamous Cell Carcinoma, Esophageal 26379361 disease of cellular proliferation DOID:3748 C562729 These findings indicated that functional polymorphisms miR-219-1 rs107822G > A might change individual susceptibility to Kazakh ESCC. genetics_GWAS hsa-mir-26a-1 Squamous Cell Carcinoma, Esophageal 24288122 disease of cellular proliferation DOID:3748 C562729 Taken together, these findings indicate that miRNA polymorphisms may predict prognosis in advanced ESCC patients receiving platinum-based chemotherapy. genetics_GWAS hsa-mir-26a-1 Squamous Cell Carcinoma, Esophageal 23792053 disease of cellular proliferation DOID:3748 C562729 These findings indicated that functional polymorphism miR-196a2 rs11614913 T > C might contribute to decreased ESCC risk among women patients and patients who never smoking or drinking. However, our results were obtained with a limited sample size. Future larger studies with other ethnic populations and tissue-specific biological characterization are required to confirm current findings. genetics_GWAS hsa-mir-27a Squamous Cell Carcinoma, Esophageal 23792053 disease of cellular proliferation DOID:3748 C562729 These findings indicated that functional polymorphism miR-196a2 rs11614913 T > C might contribute to decreased ESCC risk among women patients and patients who never smoking or drinking. However, our results were obtained with a limited sample size. Future larger studies with other ethnic populations and tissue-specific biological characterization are required to confirm current findings. genetics_GWAS hsa-mir-34b Squamous Cell Carcinoma, Esophageal 24945256 disease of cellular proliferation DOID:3748 C562729 Pri-miR-124 rs531564 and pri-miR-34b/c rs4938723 polymorphisms are associated with decreased risk of esophageal squamous cell carcinoma in Chinese populations. genetics_GWAS hsa-mir-34c Squamous Cell Carcinoma, Esophageal 24945256 disease of cellular proliferation DOID:3748 C562729 Pri-miR-124 rs531564 and pri-miR-34b/c rs4938723 polymorphisms are associated with decreased risk of esophageal squamous cell carcinoma in Chinese populations. genetics_GWAS hsa-mir-423 Squamous Cell Carcinoma, Esophageal 24205249 disease of cellular proliferation DOID:3748 C562729 MicroRNA polymorphisms and environmental smoke exposure as risk factors for oesophageal squamous cell carcinoma. genetics_GWAS hsa-mir-423 Squamous Cell Carcinoma, Esophageal 26518769 disease of cellular proliferation DOID:3748 C562729 Four SNPs including miR-196a2 rs11614913, miR-146a rs2910164, miR-499 rs3746444, and miR-423 rs6505162 were selected with comprehensive collection strategy and genotyped using the SNaPshot Multiplex System. genetics_GWAS hsa-mir-4293 Squamous Cell Carcinoma, Esophageal 26055141 disease of cellular proliferation DOID:3748 C562729 miR-449b rs10061133 and miR-4293 rs12220909 polymorphisms are associated with decreased esophageal squamous cell carcinoma in a Chinese population. genetics_GWAS hsa-mir-449b Squamous Cell Carcinoma, Esophageal 26055141 disease of cellular proliferation DOID:3748 C562729 miR-449b rs10061133 and miR-4293 rs12220909 polymorphisms are associated with decreased esophageal squamous cell carcinoma in a Chinese population. genetics_GWAS hsa-mir-483 Squamous Cell Carcinoma, Esophageal 27420938 disease of cellular proliferation DOID:3748 C562729 SNP at miR-483-5p-binding site in the 3'-untranslated region of the BSG gene is associated with susceptibility to esophageal cancer in a Chinese population. genetics_GWAS hsa-mir-499 Squamous Cell Carcinoma, Esophageal 23792053 disease of cellular proliferation DOID:3748 C562729 These findings indicated that functional polymorphism miR-196a2 rs11614913 T > C might contribute to decreased ESCC risk among women patients and patients who never smoking or drinking. However, our results were obtained with a limited sample size. Future larger studies with other ethnic populations and tissue-specific biological characterization are required to confirm current findings. genetics_GWAS hsa-mir-526b Squamous Cell Carcinoma, Esophageal 27583835 disease of cellular proliferation DOID:3748 C562729 A genetic polymorphism at miR-526b binding-site in the lincRNA-NR_024015 exon confers risk of esophageal squamous cell carcinoma in a population of North China. genetics_GWAS hsa-mir-608 Squamous Cell Carcinoma, Esophageal 24770678 disease of cellular proliferation DOID:3748 C562729 The hereditary genetic polymorphisms of mir-608, RAN, and GEMIN4 can serve as predictors for clinical outcome in ESCC patients treated with concurrent chemoradiotherapy. genetics_GWAS hsa-mir-149 Squamous Cell Carcinoma, Head and Neck 23272122 disease of cellular proliferation DOID:5520 C76.0 C535575 The Association between Genetic Polymorphism and the Processing Efficiency of miR-149 Affects the Prognosis of Patients with Head and Neck Squamous Cell Carcinoma genetics_GWAS hsa-mir-149 Squamous Cell Carcinoma, Head and Neck 27515039 disease of cellular proliferation DOID:5520 C76.0 C535575 However, no significant association was detected between the other three SNPs (miR-149 rs2292832, miR-146a rs2910164, and miR-608 rs4919510) and HNSCC risk. genetics_GWAS hsa-mir-184 Squamous Cell Carcinoma, Head and Neck 21934093 disease of cellular proliferation DOID:5520 C76.0 C535575 The authors found that, compared with the rs8126 TT (a SNP of miR-184 Binding Site in TNFAIP2) genotype, the variant C allele were associated with increased SCCHN risk in an allele-dose response manner (adjusted odds ratio=1.48 and 95% confidence interval=1.06-2.05 for CC, respectively; P(trend)=0.009). genetics_GWAS hsa-mir-21 Squamous Cell Carcinoma, Head and Neck 24327270 disease of cellular proliferation DOID:5520 C76.0 C535575 CLU is a specific, functional target of oncogenic miRNA-21 in HNSCCs. CLU-1 isoform is the predominant growth-suppressive variant targeted by miRNA-21. genetics_GWAS hsa-mir-499 Squamous Cell Carcinoma, Head and Neck 20549817 disease of cellular proliferation DOID:5520 C76.0 C535575 Of the 4 SNPs that were studied, the hsa-mir-499 AG and GG genotypes were associated with a reduced risk of SCCHN genetics_GWAS hsa-mir-146a Squamous Cell Carcinoma, Oral 22182931 disease of cellular proliferation DOID:0050866 This study identifies that areca nut extract, TNFalpha and TGFbeta up-regulates miR-146a in OSCC cells. The increased expression of miR-146a enhanced the oncogenicity of OSCC cells. In addition, a G to C polymorphism (rs2910164), which is located in the pre-miR-146a and has been associated with functional alterations in miR-146a, was significantly more prevalent among OSCC patients having more advanced nodal involvement. Our analysis also suggested a higher miR-146a expression in OSCC tissues of patients carrying C polymorphism. The present study concluded a higher prevalence of the pre-mir-146a C-variant was associated with OSCC progression in patients with this disease. genetics_GWAS hsa-mir-146a Squamous Cell Carcinoma, Oral 26214637 disease of cellular proliferation DOID:0050866 The miR-146a rs2910164 polymorphism is associated with increased risk for cervical and skin SCC. In contrast, rs2910164 in miR-146a is related to decreased risk for nasopharyngeal and oral SCC. genetics_GWAS hsa-mir-149 Squamous Cell Carcinoma, Oral 26625766 disease of cellular proliferation DOID:0050866 Our study suggests that miR-196a2C>T and miR-149C>T polymorphisms may play crucial roles in the development of OSCC in South Indian subjects. genetics_GWAS hsa-mir-149 Squamous Cell Carcinoma, Oral 29103762 disease of cellular proliferation DOID:0050866 miRNA genetic variants: As potential diagnostic biomarkers for oral cancer. genetics_GWAS hsa-mir-499a Squamous Cell Carcinoma, Oral 22761899 disease of cellular proliferation DOID:0050866 This study determined that a significant association of miRNA499 with CC genotype, as compared to the subjects with TT genotype, had a higher risk of oral squamous cell carcinoma. genetics_GWAS hsa-mir-499b Squamous Cell Carcinoma, Oral 22761899 disease of cellular proliferation DOID:0050866 This study determined that a significant association of miRNA499 with CC genotype, as compared to the subjects with TT genotype, had a higher risk of oral squamous cell carcinoma. genetics_GWAS hsa-mir-122 Stroke 29145255 I64 D020521 601367 HP:0001297 Functional polymorphism rs3783553 in the 3'-untranslated region of IL-1A increased the risk of ischemic stroke genetics_GWAS hsa-mir-410 Stroke 24990426 I64 D020521 601367 HP:0001297 We report a novel association between a microRNA target site variant and stroke incidence, which is modulated by diet in terms of decreasing triglycerides and possibly stroke risk in rs13702 C allele carriers after a high-unsaturated fat MedDiet intervention. genetics_GWAS hsa-let-7 Stroke, Ischemic 27530126 I63.9 HP:0002140 An rs13293512 polymorphism in the promoter of let-7 is associated with a reduced risk of ischemic stroke. genetics_GWAS hsa-mir-1203 Stroke, Ischemic 28171870 I63.9 HP:0002140 Methylene Tetrahydrofolate Reductase (MTHFR) rs868014 Polymorphism Regulated by miR-1203 Associates with Risk and Short Term Outcome of Ischemic Stroke. genetics_GWAS hsa-mir-130a Stroke, Ischemic 27246008 I63.9 HP:0002140 Association of miR-34a, miR-130a, miR-150 and miR-155 polymorphisms with the risk of ischemic stroke genetics_GWAS hsa-mir-130b Stroke, Ischemic 27603512 I63.9 HP:0002140 Association of the Single Nucleotide Polymorphisms in microRNAs 130b, 200b, and 495 with Ischemic Stroke Susceptibility and Post-Stroke Mortality. genetics_GWAS hsa-mir-146a Stroke, Ischemic 24952884 I63.9 HP:0002140 miR-146a and miR-196a2 polymorphisms in patients with ischemic stroke in the northern Chinese Han population. genetics_GWAS hsa-mir-146a Stroke, Ischemic 26608782 I63.9 HP:0002140 Although the 3 SNPs might be associated with IS, the association varied significantly in different countries. genetics_GWAS hsa-mir-150 Stroke, Ischemic 27246008 I63.9 HP:0002140 Association of miR-34a, miR-130a, miR-150 and miR-155 polymorphisms with the risk of ischemic stroke genetics_GWAS hsa-mir-155 Stroke, Ischemic 27246008 I63.9 HP:0002140 Association of miR-34a, miR-130a, miR-150 and miR-155 polymorphisms with the risk of ischemic stroke genetics_GWAS hsa-mir-196a-2 Stroke, Ischemic 26608782 I63.9 HP:0002140 Although the 3 SNPs might be associated with IS, the association varied significantly in different countries. genetics_GWAS hsa-mir-196a-2 Stroke, Ischemic 24952884 I63.9 HP:0002140 miR-146a and miR-196a2 polymorphisms in patients with ischemic stroke in the northern Chinese Han population. genetics_GWAS hsa-mir-199a Stroke, Ischemic 28234972 I63.9 HP:0002140 the +936C/T variants significantly increased the risk of poorer stroke outcome by affecting the bindings of miR-199a and miR-199b to VEGF mRNA at the rs30250340 polymorphic site genetics_GWAS hsa-mir-199b Stroke, Ischemic 28234972 I63.9 HP:0002140 the +936C/T variants significantly increased the risk of poorer stroke outcome by affecting the bindings of miR-199a and miR-199b to VEGF mRNA at the rs30250340 polymorphic site genetics_GWAS hsa-mir-200b Stroke, Ischemic 27603512 I63.9 HP:0002140 Association of the Single Nucleotide Polymorphisms in microRNAs 130b, 200b, and 495 with Ischemic Stroke Susceptibility and Post-Stroke Mortality. genetics_GWAS hsa-mir-34a Stroke, Ischemic 27246008 I63.9 HP:0002140 Association of miR-34a, miR-130a, miR-150 and miR-155 polymorphisms with the risk of ischemic stroke genetics_GWAS hsa-mir-495 Stroke, Ischemic 27603512 I63.9 HP:0002140 Association of the Single Nucleotide Polymorphisms in microRNAs 130b, 200b, and 495 with Ischemic Stroke Susceptibility and Post-Stroke Mortality. genetics_GWAS hsa-mir-499 Stroke, Ischemic 26608782 I63.9 HP:0002140 Although the 3 SNPs might be associated with IS, the association varied significantly in different countries. genetics_GWAS hsa-mir-618 Stroke, Ischemic 27011381 I63.9 HP:0002140 Our findings suggest that miR-618 SNP rs2682818 may play an important role in the recurrence of ischemic stroke. genetics_GWAS hsa-mir-146a Systemic Lupus Erythematosus 21738483 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 A functional variant in microRNA-146a promoter modulates its expression and confers disease risk for systemic lupus erythematosus. genetics_GWAS hsa-mir-146a Systemic Lupus Erythematosus 22218224 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 The SNP (rs2431697) was associated with the microRNA-146a, where the risk allele correlates with lower expression of the miRNA. genetics_GWAS hsa-mir-146a Systemic Lupus Erythematosus 24803388 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 Association of miR-146a polymorphisms with systemic lupus erythematosus: a meta-analysis. genetics_GWAS hsa-mir-146a Systemic Lupus Erythematosus 25218914 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 The present meta-analysis suggests important roles for the mir-499 rs3746444 polymorphism in RA, especially in the Caucasian population and for miR-146a rs57095329 polymorphism in SLE. genetics_GWAS hsa-mir-569 Systemic Lupus Erythematosus 21162035 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 Association of a functional polymorphism in the 3' untranslated region of SPI1 with systemic lupus erythematosus. genetics_GWAS hsa-mir-569 Systemic Lupus Erythematosus 21360505 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 rs1057233 alters a target sequence for microRNA hsa-miR-569 (miR-569). genetics_GWAS hsa-mir-146a Thyroid Neoplasms 17468766 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 somatic mutations altering binding sites for miR-221, miR-222 and miR-146 have been observed in the 3'UTR of the KIT oncogene in papillary thyroid carcinoma. genetics_GWAS hsa-mir-146a Thyroid Neoplasms 19164563 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 miR-146a: SNP rs2910164 contribute to thyroid cancer genetics_GWAS hsa-mir-146a Thyroid Neoplasms 23451063 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Association between the rs2910164 Polymorphism in Pre-Mir-146a Sequence and Thyroid Carcinogenesis genetics_GWAS hsa-mir-146a Thyroid Neoplasms 28899898 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 The rs2910164 variant in MIR146A is significantly associated with DTC genetics_GWAS hsa-mir-146a Thyroid Neoplasms 18474871 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Thus, our data suggest that a common polymorphism in pre-miR-146a affects the miR expression, contributes to the genetic predisposition to PTC, and plays a role in the tumorigenesis through somatic mutation. genetics_GWAS hsa-mir-146a Thyroid Neoplasms 21978540 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Despite some limitations, this meta-analysis suggests that the miR-146a G allele is a low-penetrant risk factor for papillary thyroid carcinoma development. genetics_GWAS hsa-mir-146b Thyroid Neoplasms 17468766 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 somatic mutations altering binding sites for miR-221, miR-222 and miR-146 have been observed in the 3'UTR of the KIT oncogene in papillary thyroid carcinoma. genetics_GWAS hsa-mir-149 Thyroid Neoplasms 25405731 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Rs2292832 was possibly involved in the susceptibility and local progression of PTC in Chinese patients, by altering the expression level of mir-149-5p and its target genes. genetics_GWAS hsa-mir-221 Thyroid Neoplasms 17468766 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 somatic mutations altering binding sites for miR-221, miR-222 and miR-146 have been observed in the 3'UTR of the KIT oncogene in papillary thyroid carcinoma. genetics_GWAS hsa-mir-222 Thyroid Neoplasms 17468766 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 somatic mutations altering binding sites for miR-221, miR-222 and miR-146 have been observed in the 3'UTR of the KIT oncogene in papillary thyroid carcinoma. genetics_GWAS hsa-mir-1273d Tooth Agenesis 27362534 gastrointestinal system disease DOID:0050591 K00.0 D000848 PS106600 HP:0001592 our findings indicate that rs15705 and rs317250 are associated with the susceptibility of non-syndromic tooth agenesis by possibly affecting miRNAs and mRNA interaction. genetics_GWAS hsa-mir-4639 Tooth Agenesis 27362534 gastrointestinal system disease DOID:0050591 K00.0 D000848 PS106600 HP:0001592 rs15705 and rs317250 are associated with the susceptibility of non-syndromic tooth agenesis by possibly affecting miRNAs and mRNA interaction. genetics_GWAS hsa-mir-189 Tourette Syndrome 16224024 disease of mental health DOID:11119 F95.2 D005879 137580 we identified a frameshift mutation and two independent occurrences of the identical variant in the binding site for microRNA hsa-miR-189 genetics_GWAS hsa-mir-146a Tuberculosis, Pulmonary 25650003 disease by infectious agent DOID:2957 A15 D014397 Association of the miR-146a, miR-149, miR-196a2 and miR-499 polymorphisms with susceptibility to pulmonary tuberculosis in the Chinese Uygur, Kazak and Southern Han populations. genetics_GWAS hsa-mir-146a Tuberculosis, Pulmonary 21524676 disease by infectious agent DOID:2957 A15 D014397 A polymorphism (rs2910164 G>C, in miR-146a) indicated an association with PTB risk in both Tibetan (p = 0.031) and Han (p = 0.000) populations. However, the role of the G allele of rs2910164, like the C allele in rs3746444, differed in the Tibetan (OR = 1.509, p < 0.05) and Han (OR = 0.575, p < 0.05) groups. genetics_GWAS hsa-mir-149 Tuberculosis, Pulmonary 25650003 disease by infectious agent DOID:2957 A15 D014397 Association of the miR-146a, miR-149, miR-196a2 and miR-499 polymorphisms with susceptibility to pulmonary tuberculosis in the Chinese Uygur, Kazak and Southern Han populations. genetics_GWAS hsa-mir-196a-2 Tuberculosis, Pulmonary 25650003 disease by infectious agent DOID:2957 A15 D014397 Association of the miR-146a, miR-149, miR-196a2 and miR-499 polymorphisms with susceptibility to pulmonary tuberculosis in the Chinese Uygur, Kazak and Southern Han populations. genetics_GWAS hsa-mir-499 Tuberculosis, Pulmonary 25650003 disease by infectious agent DOID:2957 A15 D014397 Association of the miR-146a, miR-149, miR-196a2 and miR-499 polymorphisms with susceptibility to pulmonary tuberculosis in the Chinese Uygur, Kazak and Southern Han populations. genetics_GWAS hsa-mir-499a Tuberculosis, Pulmonary 21524676 disease by infectious agent DOID:2957 A15 D014397 There was no association between rs3746444 (in hsa-mir-499) and PTB risk (p = 0.118) in the Han population, but subjects carrying the C allele exhibited decreased PTB risk (odds ratio [OR] = 0.403 [95% confidence interval (95% CI) 0.278-0.583]). There was an association between rs3746444 and PTB in the Tibetan population, and individuals carrying the C allele exhibited increased PTB risk (OR = 1.870 [95% CI 1.218-2.871]). genetics_GWAS hsa-mir-146a Urinary Bladder Cancer 22846912 urinary system disease DOID:11054 C67 D001749 109800 miR-146a rs2910164 C allele inhibited cell proliferation and significantly downregulates expression of IRAK1 and TRAF6 in bladder cancer cells. genetics_GWAS hsa-mir-146a Urinary Bladder Cancer 21529907 urinary system disease DOID:11054 C67 D001749 109800 Polymorphism (rs2910164) of the pre-miR-146a is associated with risk of cervical cancer in a Chinese population. The subjects carrying GG homozygote had a 1.496-foldincreased risk than those carrying CG/CC genotypes. The carriers of GG genotype had obviously more reduced miR-146a expression level compared with the carriers of CC genotype. genetics_GWAS hsa-mir-196a-2 Urinary Bladder Cancer 21345130 urinary system disease DOID:11054 C67 D001749 109800 Our results showed that the heterozygous genotype of rs11614913 (hsa-mir-196a2 C>T rs11614913) was higher in cases than controls but the results were marginally significant (p=0.055; odds ratio, 1.44). genetics_GWAS hsa-mir-196b Urinary Bladder Cancer 21345130 urinary system disease DOID:11054 C67 D001749 109800 Our results showed that the heterozygous genotype of rs11614913 (hsa-mir-196a2 C>T rs11614913) was higher in cases than controls but the results were marginally significant (p=0.055; odds ratio, 1.44). genetics_GWAS hsa-mir-218-1 Urinary Bladder Cancer 20163849 urinary system disease DOID:11054 C67 D001749 109800 miR-218:Polymorphisms involved in the miR-218-LAMB3 pathway and susceptibility of cervical cancer genetics_GWAS hsa-mir-218-1 Urinary Bladder Cancer 23320911 urinary system disease DOID:11054 C67 D001749 109800 The pri-miR-218 rs11134527 SNP was significantly associated with the risk of cervical carcinoma in Eastern Chinese women genetics_GWAS hsa-mir-218-2 Urinary Bladder Cancer 20163849 urinary system disease DOID:11054 C67 D001749 109800 miR-218:Polymorphisms involved in the miR-218-LAMB3 pathway and susceptibility of cervical cancer genetics_GWAS hsa-mir-218-2 Urinary Bladder Cancer 23320911 urinary system disease DOID:11054 C67 D001749 109800 The pri-miR-218 rs11134527 SNP was significantly associated with the risk of cervical carcinoma in Eastern Chinese women genetics_GWAS hsa-mir-7-1 Urinary Bladder Cancer 22768238 urinary system disease DOID:11054 C67 D001749 109800 A microRNA-7 binding site polymorphism (1010A/G) in HOXB5 leads to differential gene expression in bladder cancer. genetics_GWAS hsa-mir-7-2 Urinary Bladder Cancer 22768238 urinary system disease DOID:11054 C67 D001749 109800 A microRNA-7 binding site polymorphism (1010A/G) in HOXB5 leads to differential gene expression in bladder cancer. genetics_GWAS hsa-mir-7-3 Urinary Bladder Cancer 22768238 urinary system disease DOID:11054 C67 D001749 109800 A microRNA-7 binding site polymorphism (1010A/G) in HOXB5 leads to differential gene expression in bladder cancer. genetics_GWAS hsa-mir-146a Uveitis 24658012 nervous system disease DOID:13141 H20.9 D014605 This study shows that miR-146a and Ets-1 are both associated with pediatric uveitis in Han Chinese. SNP rs10893872 may affect the genetic predisposition to pediatric uveitis by modulating expression of Ets-1. genetics_GWAS hsa-mir-1 Vascular Hypertrophy 17381315 we have identified an A-to-G transition in the 3'UTR of the GDF8 gene that reveals an illegitimate target site for microRNAs miR-1 and miR-206 that are highly expressed in skeletal muscle. genetics_GWAS hsa-mir-206 Vascular Hypertrophy 17381315 we have identified an A-to-G transition in the 3'UTR of the GDF8 gene that reveals an illegitimate target site for microRNAs miR-1 and miR-206 that are highly expressed in skeletal muscle. genetics_GWAS hsa-mir-570 Viral Infectious Disease 26199425 disease by infectious agent DOID:934 A94 D001102 it was demonstrated that human CYP2E1 was regulated by miR-570 in a genotype-dependent manner. This report describes the first proof that SNP in 3'-UTR of human P450 affects binding of miRNA to modulate the expression in the liver. genetics_GWAS hsa-mir-196a-2 Vitiligo 23433405 immune system disease DOID:12306 L80 D014820 HP:0001045 A Single Nucleotide Polymorphism of miR-196a-2 and Vitiligo: An Association Study and Functional Analysis in a Han Chinese Population genetics_GWAS hsa-mir-196a-2 Vitiligo 25896941 immune system disease DOID:12306 L80 D014820 HP:0001045 miR-196a-2 rs11614913 polymorphism is associated with vitiligo by affecting heterodimeric molecular complexes of Tyr and Tyrp1. genetics_knock down_promote hsa-mir-21 Acute Kidney Failure 25844699 urinary system disease DOID:3021 N17.9 D058186 HP:0001919 Knockdown of miR-21 upregulated its target effectors programmed cell death protein 4 and phosphatase and tensin homolog deleted on chromosome 10 expression, resulted in an increase in apoptosis, and exacerbated lipopolysaccharide-induced acute kidney injury. genetics_knock down_promote hsa-mir-29a Alzheimer Disease 18434550 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 loss genetics_knock down_promote hsa-mir-29b-1 Alzheimer Disease 18434550 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 loss genetics_knock down_promote hsa-mir-206 Amyotrophic Lateral Sclerosis 24664281 nervous system disease DOID:332 G12.21 D000690 PS105400 HP:0007354 in mutant mice lacking miR-206, reinnervation is impaired following nerve injury and loss of NMJs is accelerated in a mouse model of amyotrophic lateral sclerosis (ALS). genetics_knock down_promote hsa-mir-17 Atrial Fibrillation 24927531 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 miR-17-92 and miR-106b-25 directly repress genes, such as Shox2 and Tbx3, that are required for sinoatrial node development.Together, to our knowledge, these findings provide the first genetic evidence for an miR loss-of-function that increases atrial fibrillation susceptibility. genetics_knock down_promote hsa-mir-18 Atrial Fibrillation 24927531 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 miR-17-92 and miR-106b-25 directly repress genes, such as Shox2 and Tbx3, that are required for sinoatrial node development.Together, to our knowledge, these findings provide the first genetic evidence for an miR loss-of-function that increases atrial fibrillation susceptibility. genetics_knock down_promote hsa-mir-19a Atrial Fibrillation 24927531 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 miR-17-92 and miR-106b-25 directly repress genes, such as Shox2 and Tbx3, that are required for sinoatrial node development.Together, to our knowledge, these findings provide the first genetic evidence for an miR loss-of-function that increases atrial fibrillation susceptibility. genetics_knock down_promote hsa-mir-19b-1 Atrial Fibrillation 24927531 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 miR-17-92 and miR-106b-25 directly repress genes, such as Shox2 and Tbx3, that are required for sinoatrial node development.Together, to our knowledge, these findings provide the first genetic evidence for an miR loss-of-function that increases atrial fibrillation susceptibility. genetics_knock down_promote hsa-mir-20a Atrial Fibrillation 24927531 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 miR-17-92 and miR-106b-25 directly repress genes, such as Shox2 and Tbx3, that are required for sinoatrial node development.Together, to our knowledge, these findings provide the first genetic evidence for an miR loss-of-function that increases atrial fibrillation susceptibility. genetics_knock down_promote hsa-mir-92-1 Atrial Fibrillation 24927531 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 miR-17-92 and miR-106b-25 directly repress genes, such as Shox2 and Tbx3, that are required for sinoatrial node development.Together, to our knowledge, these findings provide the first genetic evidence for an miR loss-of-function that increases atrial fibrillation susceptibility. genetics_knock down_promote hsa-mir-181 Autism Spectrum Disorder 27017280 disease of mental health DOID:0060041 F84.0 D000067877 209850 HP:0000729 this loss-of miR-181c function resulted in enhanced neurite sprouting and reduced synaptogenesis genetics_knock down_promote hsa-mir-125b-1 Breast Neoplasms 14973191 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 deletion genetics_knock down_promote hsa-mir-133a-1 Breast Neoplasms 22292984 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Loss of miR-133a expression associated with poor survival of breast cancer and restoration of miR-133a expression inhibited breast cancer cell growth and invasion. genetics_knock down_promote hsa-mir-133a-2 Breast Neoplasms 22292984 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Loss of miR-133a expression associated with poor survival of breast cancer and restoration of miR-133a expression inhibited breast cancer cell growth and invasion. genetics_knock down_promote hsa-mir-15a Breast Neoplasms 17012848 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Later on, deletion of mir-16-1 and mir-15a deletion were also identified in epithelial tumors, such as pituitary adenomas, ovarian and breast cancer. genetics_knock down_promote hsa-mir-17 Breast Neoplasms 16940181 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The genomic location of Mir-17-5p also undergoesloss of heterozygosity in different types of cancer, including breast cancer. genetics_knock down_promote hsa-mir-200a Breast Neoplasms 24280074 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Loss of microRNA-200a expression correlates with tumor progression in breast cancer. genetics_knock down_promote hsa-mir-218-1 Breast Neoplasms 22898079 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Silencing of miRNA-218 promotes migration and invasion of breast cancer via Slit2-Robo1 pathway. genetics_knock down_promote hsa-mir-218-2 Breast Neoplasms 22898079 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Silencing of miRNA-218 promotes migration and invasion of breast cancer via Slit2-Robo1 pathway. genetics_knock down_promote hsa-mir-7 Breast Neoplasms 25532106 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Suppression of miR-7 in the MCF-7 cell line resulted in enhanced colony formation activity but not cell migration genetics_knock down_promote hsa-mir-29c Carcinoma, Embryonal 26848028 disease of cellular proliferation DOID:3308 D018236 HP:0002898 Inhibition of miR鈥?9c promoted proliferation, and suppressed the apoptosis and differentiation of P19 cells. genetics_knock down_promote hsa-mir-101 Carcinoma, Esophageal 25400732 disease of cellular proliferation DOID:1107 C15.9 D004938 133239 HP:0011459 decreased expression of miR-101 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein. genetics_knock down_promote hsa-mir-100 Carcinoma, Hepatocellular 25361001 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Downregulation of microRNA-100 enhances the ICMT-Rac1 signaling and promotes metastasis of hepatocellular carcinoma cells. genetics_knock down_promote hsa-mir-1-1 Carcinoma, Hepatocellular 18593903 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-1: silenced genetics_knock down_promote hsa-mir-1-2 Carcinoma, Hepatocellular 18593903 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-1: silenced genetics_knock down_promote hsa-mir-126 Carcinoma, Hepatocellular 28639884 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9. genetics_knock down_promote hsa-mir-142 Carcinoma, Hepatocellular 28177895 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Over-expression of Thrombospondin 4 correlates with loss of miR-142 and contributes to migration and vascular invasion of advanced hepatocellular carcinoma. genetics_knock down_promote hsa-mir-145 Carcinoma, Hepatocellular 24690171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Our results demonstrated that miR-145 could inhibit HCC through targeting IRS1 and its downstream signaling, implicating the loss of miR-145 regulation may be a potential molecular mechanism causing aberrant oncogenic signaling in HCC. genetics_knock down_promote hsa-mir-17 Carcinoma, Hepatocellular 15944709 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 loss of heterozygosity of this cluster genetics_knock down_promote hsa-mir-18a Carcinoma, Hepatocellular 15944709 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 loss of heterozygosity of this cluster genetics_knock down_promote hsa-mir-199a-1 Carcinoma, Hepatocellular 17188425 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 This region encodes miRNA-199a-1 (19p13.2), whose expression levels are lower in HCC compared to nontumor liver [59] and is deleted in several other tumor types. genetics_knock down_promote hsa-mir-19a Carcinoma, Hepatocellular 15944709 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 loss of heterozygosity of this cluster genetics_knock down_promote hsa-mir-19b-1 Carcinoma, Hepatocellular 15944709 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 loss of heterozygosity of this cluster genetics_knock down_promote hsa-mir-20a Carcinoma, Hepatocellular 15944709 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 loss of heterozygosity of this cluster genetics_knock down_promote hsa-mir-21 Carcinoma, Hepatocellular 26282675 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 microRNA-21 knockdown led to increased HBP1 and p53 and subsequently reduced lipogenesis and delayed G1/S transition, and the additional treatment of HBP1-siRNA antagonised the effect of microRNA-21-ASO, suggesting that HBP1 mediated the inhibitory effects of microRNA-21-ASO on both hepatic lipid accumulation and hepatocarcinogenesis. genetics_knock down_promote hsa-mir-320a Carcinoma, Hepatocellular 28288874 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Loss of exosomal miR-320a from cancer-associated fibroblasts contributes to HCC proliferation and metastasis. genetics_knock down_promote hsa-mir-505 Carcinoma, Hepatocellular 27259809 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 the up-regulation of miR-505 suppressed, whereas the down-regulation of miR-505 promoted proliferation, invasion and epithelial-mesenchymal transition in MHCC97. genetics_knock down_promote hsa-mir-15a Carcinoma, Lung, Non-Small-Cell 29551936 C34.90 D002289 HP:0030358 Knocking down MiR-15a expression promotes the occurrence and development and induces the EMT of NSCLC cells in vitro genetics_knock down_promote hsa-mir-424 Carcinoma, Lung, Non-Small-Cell 27500472 C34.90 D002289 HP:0030358 It was found that down-regulation of miR-424-3p was pronouncedly associated with NSCLC progression and overall prognosis; genetics_knock down_promote hsa-mir-101-1 Carcinoma, Lung, Non-Small-Cell 21993632 C34.90 D002289 HP:0030358 Down-regulation of miR-101 was associated with overexpression of Mcl-1 mRNA in NSCLC tissue when compared with corresponding normal tissue, with a negative correlation (r = -0.724, P < 0.01). MiR-101 expression was significantly associated with pathological stage (P = 0.004) and lymph node involvement (P = 0.012). Overexpression of Mcl-1 was associated with pathological grade (P = 0.022) and lymph node involvement (P = 0.017). A comparison of survival curves of low versus high expressers of miR-101 and Mcl-1 revealed a highly significant difference in NSCLC (P < 0.05), which suggests that reduced expression of miR-101 versus overexpression of Mcl-1 is associated with a poorer prognosis. genetics_knock down_promote hsa-mir-101-2 Carcinoma, Lung, Non-Small-Cell 21993632 C34.90 D002289 HP:0030358 Down-regulation of miR-101 was associated with overexpression of Mcl-1 mRNA in NSCLC tissue when compared with corresponding normal tissue, with a negative correlation (r = -0.724, P < 0.01). MiR-101 expression was significantly associated with pathological stage (P = 0.004) and lymph node involvement (P = 0.012). Overexpression of Mcl-1 was associated with pathological grade (P = 0.022) and lymph node involvement (P = 0.017). A comparison of survival curves of low versus high expressers of miR-101 and Mcl-1 revealed a highly significant difference in NSCLC (P < 0.05), which suggests that reduced expression of miR-101 versus overexpression of Mcl-1 is associated with a poorer prognosis. genetics_knock down_promote hsa-mir-214 Carcinoma, Nasopharyngeal 24465927 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Knockdown of miR-214 promotes apoptosis and inhibits cell proliferation in nasopharyngeal carcinoma. genetics_knock down_promote hsa-mir-29b Carcinoma, Renal Cell 26823729 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Inhibition of miR-29b expression could promote apoptosis, and inhibit proliferation and invasion ability in SN12-PM6 cells. genetics_knock down_promote hsa-mir-146b Carcinoma, Thyroid, Papillary 25819770 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 The results showed that PTC cells overexpress miR-146b and miR-222 in exosomes; and that factors released by both normal thyroid and PTC cells alter proliferation of other cells in a complex manner. The intercellular interactions were likely conferred in part by exosomal miRNA, which can potentially be developed as biomarkers of PTC recurrence. genetics_knock down_promote hsa-mir-222 Carcinoma, Thyroid, Papillary 25819770 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 The results showed that PTC cells overexpress miR-146b and miR-222 in exosomes; and that factors released by both normal thyroid and PTC cells alter proliferation of other cells in a complex manner. The intercellular interactions were likely conferred in part by exosomal miRNA, which can potentially be developed as biomarkers of PTC recurrence. genetics_knock down_promote hsa-mir-195 Cervical Neoplasms 26511972 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 reducing the endogenous miR-195 level by miR-195 inhibitor promoted the proliferation of cervical cancer cells. genetics_knock down_promote hsa-mir-370 Cholangiocarcinoma 23110045 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 Silencing of miR-370 in human cholangiocarcinoma by allelic loss and interleukin-6 induced maternal to paternal epigenotype switch genetics_knock down_promote hsa-mir-101-1 Colon Neoplasms 22930392 D12.6 D003110 HP:0100273 Loss of miR-101 Expression Promotes Wnt/beta-Catenin Signalling Pathway Activation and Malignancy in Colon Cancer Cells. genetics_knock down_promote hsa-mir-4282 Colorectal Carcinoma 27120047 disease of cellular proliferation DOID:0080199 C19 D015179 114500 It was found that miR-4282 inhibition promoted cell growth, migration and invasion (P<0.05) of HT29 and HCT116 colorectal carcinoma cells while miR-4282 overexpression suppressed cell growth and mobility (P<0.05). genetics_knock down_promote hsa-mir-622 Colorectal Carcinoma 26333174 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-622 inhibited tumor proliferation and migration in vitro. genetics_knock down_promote hsa-mir-34a Diabetes Mellitus 25483877 disease of metabolism DOID:9351 E10-E14 D003920 222100 HP:0000819 Knockdown of miR-34a slightly decreased proliferation, but as apoptosis and NO synthesis were highly reduced, miR-34a may be further investigated as a therapeutic target to reduce 尾-cell death and dysfunction. genetics_knock down_promote hsa-mir-150 Diabetic Retinopathy 27304911 nervous system disease DOID:8947 E10-11.31 D003930 deletion of miR-150 significantly increased the retinal pathological angiogenesis genetics_knock down_promote hsa-mir-148a Endometrial Neoplasms 22890324 reproductive system disease DOID:1380 C54.1 D016889 608089 Silencing of miR-148a in cancer-associated fibroblasts results in WNT10B-mediated stimulation of tumor cell motility. genetics_knock down_promote hsa-mir-101-1 Gastric Neoplasms 22450781 disease of cellular proliferation DOID:10534 C16 D013274 137215 Lack of microRNA-101 causes E-cadherin functional deregulation through EZH2 upregulation in intestinal gastric cancer. genetics_knock down_promote hsa-mir-486 Gastric Neoplasms 21415212 disease of cellular proliferation DOID:10534 C16 D013274 137215 Genomic Loss of miR-486 Regulates Tumor Progression and the OLFM4 Anti-apoptotic Factor in Gastric Cancer. genetics_knock down_promote hsa-mir-124 Glioblastoma 26993295 D005909 HP:0100843 inhibitor of miR-124 promoted the expression of STAT3 and cell proliferation. genetics_knock down_promote hsa-mir-124-1 Glioma 22253443 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Loss of brain-enriched miR-124 enhances the stem-like traits and invasiveness of glioma cells. genetics_knock down_promote hsa-mir-124-2 Glioma 22253443 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Loss of brain-enriched miR-124 enhances the stem-like traits and invasiveness of glioma cells. genetics_knock down_promote hsa-mir-124-3 Glioma 22253443 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Loss of brain-enriched miR-124 enhances the stem-like traits and invasiveness of glioma cells. genetics_knock down_promote hsa-mir-204 Glioma 23204229 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Loss of miR-204 Expression Enhances Glioma Migration and Stem Cell-like Phenotype genetics_knock down_promote hsa-mir-423 Glioma 28381178 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 miR-423-5p knockdown enhances the sensitivity of glioma stem cells to apigenin through the mitochondrial pathway. genetics_knock down_promote hsa-mir-146a Gout 29544526 musculoskeletal system disease DOID:13189 M10 D006073 HP:0001997 miR-146a provides negative feedback regulation of gouty arthritis development and lack of miR-146a enhances gouty arthritis via upregulation of TRAK6, IRAK-1, and the NALP3 inflammasome function genetics_knock down_promote hsa-mir-126 Heart Failure 23136161 I50 D006331 HP:0001635 Loss of AngiomiR-126 and 130a in Angiogenic Early Outgrowth Cells From Patients With Chronic Heart Failure: Role for Impaired In Vivo Neovascularization and Cardiac Repair Capacity genetics_knock down_promote hsa-mir-130a Heart Failure 23136161 I50 D006331 HP:0001635 Loss of AngiomiR-126 and 130a in Angiogenic Early Outgrowth Cells From Patients With Chronic Heart Failure: Role for Impaired In Vivo Neovascularization and Cardiac Repair Capacity genetics_knock down_promote hsa-mir-133a Heart Failure 26064437 I50 D006331 HP:0001635 attenuation of miR-133a contributes to the exacerbation of diabetes mediated cardiac autophagy and hypertrophy in heart failure genetics_knock down_promote hsa-mir-150 Heart Failure 25824147 I50 D006331 HP:0001635 we show that genetic deletion of miR-150 in mice causes abnormalities in cardiac structural and functional remodelling after MI. genetics_knock down_promote hsa-mir-92a-1 Hematologic Neoplasms 17011485 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 The miR-17-92 cluster is amplified in hematopoietic malignancies. genetics_knock down_promote hsa-mir-122 Hepatitis B Virus Infection 22105316 disease by infectious agent DOID:2043 B16/18 D006509 610424 Loss of MiR-122 expression in patients with hepatitis B enhances hepatitis B virus replication through cyclin G1 modulated P53 activity. genetics_knock down_promote hsa-mir-424 Hepatoblastoma 24796297 disease of cellular proliferation DOID:687 C22.2 D018197 HP:0002884 Furthermore, miR-424 or miR-503 depletion enhanced extravasation to the lungs of hepatocarcinoma cells injected in the tail vein of mice. genetics_knock down_promote hsa-mir-21 Hypertension 21920918 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 Induction of miR-21 and miR-27a may be a critical component of BMP-induced growth suppression, loss of which likely contributes to vascular cell proliferation in HPAH (Heritable pulmonary arterial hypertension). genetics_knock down_promote hsa-mir-133a Hypertrophy 26064437 D006984 attenuation of miR-133a contributes to the exacerbation of diabetes mediated cardiac autophagy and hypertrophy in heart failure genetics_knock down_promote hsa-mir-7 Hypogonadotropic Hypogonadism 28218624 endocrine system disease DOID:0090070 E23.0 PS147950 Loss of microRNA-7a2 induces hypogonadotropic hypogonadism and infertility. genetics_knock down_promote hsa-mir-23a Idiopathic Pulmonary Hypertension 25815108 I27.20 D065627 178600 Finally we found that silencing of miR23a resulted in an increase of the expression of PGC1α, as well as in its well-known regulated genes CYC, SOD, NRF2,and HO1. The results point to the utility of circulating miRNA expression as a biomarker of disease progression. genetics_knock down_promote hsa-mir-132 Inflammation 26052826 D007249 Blockage of miR-132 using miR-132 inhibitor reversed the Ach action upon LPS-induced release of inflammatory mediators and reduction in AchE protein/activity. genetics_knock down_promote hsa-mir-146a Ischemia-Reperfusion Injury 27444565 D015427 After unilateral IRI, miR-146a-/- mice exhibited more extensive tubular injury, inflammatory infiltrates, and fibrosis than wild-type mice. genetics_knock down_promote hsa-mir-146a Ischemia-Reperfusion Injury 27250735 D015427 miR146a exerts a kidney protective effect through negative regulation of acute inflammatory response genetics_knock down_promote hsa-mir-21 Ischemia-Reperfusion Injury 24098402 D015427 Our data clearly demonstrate that miR-21 is involved in IPost-mediated cardiac protection against I/R injury and dysfunction through the PTEN/Akt signaling pathway in vivo. genetics_knock down_promote hsa-mir-377 Ischemia-Reperfusion Injury 26564600 D015427 These findings indicate that HF increased miR-377 expression in the myocardium, which is detrimental to stem cell function, and transplantation of miR-377 knockdown hCD34(+) cells into ischemic myocardium promoted their angiogenic ability, attenuating left ventricular remodeling and cardiac fibrosis. genetics_knock down_promote hsa-let-7 Kaposi Sarcoma 27531260 disease of cellular proliferation DOID:8632 C46 D012514 Let-7 silencing may activate the replication of KSHV, possibly through up-regulating MAP4K4 and its downstream molecules COX-2, MMP-13, and phosphorylation of ERK1/2, finally results in the progression of Kaposi sarcoma. genetics_knock down_promote hsa-mir-29a Kidney Diseases [unspecific] 22095944 N18.9 D007674 Suppression of microRNA-29 Expression by TGF-beta1 Promotes Collagen Expression and Renal Fibrosis. genetics_knock down_promote hsa-mir-29b-1 Kidney Diseases [unspecific] 22095944 N18.9 D007674 Suppression of microRNA-29 Expression by TGF-beta1 Promotes Collagen Expression and Renal Fibrosis. genetics_knock down_promote hsa-mir-29b-2 Kidney Diseases [unspecific] 22095944 N18.9 D007674 Suppression of microRNA-29 Expression by TGF-beta1 Promotes Collagen Expression and Renal Fibrosis. genetics_knock down_promote hsa-mir-29c Kidney Diseases [unspecific] 22095944 N18.9 D007674 Suppression of microRNA-29 Expression by TGF-beta1 Promotes Collagen Expression and Renal Fibrosis. genetics_knock down_promote hsa-mir-15a Leukemia 12434020 C95 D007938 613065 HP:0001909 deletion or downregulation genetics_knock down_promote hsa-mir-15a Leukemia 16166262 C95 D007938 613065 HP:0001909 the deletion or downregulation of mir-15a results in increased expression of BCL2. genetics_knock down_promote hsa-mir-15a Leukemia 27533467 C95 D007938 613065 HP:0001909 both miR-15a deficient HSC and B1P cells are capable of repopulating irradiated recipients and produce higher numbers of B1 cells than sources with normal miR-15a/16 levels. genetics_knock down_promote hsa-mir-16-1 Leukemia 12434020 C95 D007938 613065 HP:0001909 deletion or downregulation genetics_knock down_promote hsa-mir-16-1 Leukemia 16166262 C95 D007938 613065 HP:0001909 the deletion or downregulation of mir-15a results in increased expression of BCL2. genetics_knock down_promote hsa-mir-125b Leukemia, B-Cell 29555645 C91.31 D015448 151430 physiological silencing of miR-125b is required for normal B-cell development and also acts as a mechanism of cancer suppression genetics_knock down_promote hsa-mir-125b-1 Leukemia, B-Cell 16885332 C91.31 D015448 151430 In a precursor B-cell acute lymphoblastic leukemia, an insertion of miR-125b-1 into a rearranged immunoglobulin heavy chain locus was described. genetics_knock down_promote hsa-mir-125b-1 Leukemia, B-Cell 17028302 C91.31 D015448 151430 It is of note that insertion of miR-125b-1 into a rearranged immunoglobulin heavy chain gene locus was recently reported in a patient with precursor B-cell acute lymphoblastic leukemia, though the expression miR-125b-1 was not investigated. genetics_knock down_promote hsa-mir-142 Leukemia, B-Cell 16885332 C91.31 D015448 151430 It was shown later that miR-142 is located at the chromosome 17 breakpoint and that c-Myc was rearranged under the control of the promoter of miR-142 with consequent overexpression. genetics_knock down_promote hsa-mir-15a Leukemia, B-Cell 16885332 C91.31 D015448 151430 Deleted and down-regulated in the majority of B-CLLs genetics_knock down_promote hsa-mir-16-1 Leukemia, B-Cell 16885332 C91.31 D015448 151430 Deleted and down-regulated in the majority of B-CLLs genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 24026141 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 There was a significantly decreased expression of both miRNAs in patients with biallelic deletion of the 13q14 region but only when deletions were present in 77% or more of cells, as detected by fluorescent in situ hybridization (FISH). genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 24732594 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Allele-specific loss and transcription of the miR-15a/16-1 cluster in chronic lymphocytic leukemia. genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 12434020 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 deletion or downregulation genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 17012848 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 It was found that mir-16-1 and mir-15a at 13q14 are deleted in more than 50% patients, with concurrent reduced expression in ~65% patients. Further studies demonstrated that these two miRNAs suppress BCL2 expression and may serve as tumor suppressor genes in this disease. genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 17028302 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Detailed analyses of deletion and expression status revealed these two miRNAs to be located within a 30 kb minimally deleted region in chronic lymphocytic leukemia (CLL) patients, both of which were deleted or downregulated in most CLL cases, suggesting that miR-15a and miR-16-1 may function as tumor suppressor genes. genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 17234972 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 After years of futile attemptsto identify the gene(s) in the deleted 13q14 region that participatein the pathogenesis of chronic lymphocytic leukemia, Calin etal discovered that miR-15 and miR-16 are located within thissequence and that both are downregulated in 68% of cases. genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 17531469 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 The loss-of-function of miR-15a and miR-16-1 in CLL, and perhaps other cancers as well, may contribute to malignant transformation by upregulating Bcl2 thereby preventing apoptosis. genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 17940623 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 17965831 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 miR-15a and miR-16 are often deleted from chromosome 13q14.2 in patients with B cell CLL, suggesting that these miRNAs may be involved in tumour suppression. Additionally, introduction of exogenous miR-16 into a malignant B-1 cell line resulted in increased apoptosis. genetics_knock down_promote hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 21156224 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 often absent genetics_knock down_promote hsa-mir-15b Leukemia, Lymphocytic, Chronic, B-Cell 17234972 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 After years of futile attemptsto identify the gene(s) in the deleted 13q14 region that participatein the pathogenesis of chronic lymphocytic leukemia, Calin etal discovered that miR-15 and miR-16 are located within thissequence and that both are downregulated in 68% of cases. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 24026141 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 There was a significantly decreased expression of both miRNAs in patients with biallelic deletion of the 13q14 region but only when deletions were present in 77% or more of cells, as detected by fluorescent in situ hybridization (FISH). genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 24732594 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Allele-specific loss and transcription of the miR-15a/16-1 cluster in chronic lymphocytic leukemia. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 12434020 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 deletion or downregulation genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 17012848 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 It was found that mir-16-1 and mir-15a at 13q14 are deleted in more than 50% patients, with concurrent reduced expression in ~65% patients. Further studies demonstrated that these two miRNAs suppress BCL2 expression and may serve as tumor suppressor genes in this disease. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 17028302 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Detailed analyses of deletion and expression status revealed these two miRNAs to be located within a 30 kb minimally deleted region in chronic lymphocytic leukemia (CLL) patients, both of which were deleted or downregulated in most CLL cases, suggesting that miR-15a and miR-16-1 may function as tumor suppressor genes. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 17234972 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 After years of futile attemptsto identify the gene(s) in the deleted 13q14 region that participatein the pathogenesis of chronic lymphocytic leukemia, Calin etal discovered that miR-15 and miR-16 are located within thissequence and that both are downregulated in 68% of cases. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 17531469 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 the loss-of-function of miR-15a and miR-16-1 in CLL, and perhaps other cancers as well, may contribute to malignant transformation by upregulating Bcl2 thereby preventing apoptosis. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 17940623 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 17965831 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 miR-15a and miR-16 are often deleted from chromosome 13q14.2 in patients with B cell CLL, suggesting that these miRNAs may be involved in tumour suppression. Additionally, introduction of exogenous miR-16 into a malignant B-1 cell line resulted in increased apoptosis. genetics_knock down_promote hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 21156224 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 often absent genetics_knock down_promote hsa-mir-16-2 Leukemia, Lymphocytic, Chronic, B-Cell 17234972 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 After years of futile attemptsto identify the gene(s) in the deleted 13q14 region that participatein the pathogenesis of chronic lymphocytic leukemia, Calin etal discovered that miR-15 and miR-16 are located within thissequence and that both are downregulated in 68% of cases. genetics_knock down_promote hsa-mir-16-2 Leukemia, Lymphocytic, Chronic, B-Cell 17965831 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 miR-15a and miR-16 are often deleted from chromosome 13q14.2 in patients with B cell CLL, suggesting that these miRNAs may be involved in tumour suppression. Additionally, introduction of exogenous miR-16 into a malignant B-1 cell line resulted in increased apoptosis. genetics_knock down_promote hsa-mir-29a Leukemia, Myeloid, Acute 20628397 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 miR-29a:The tumour-suppressive miR-29a/b1 cluster is regulated by CEBPA and blocked in human AML genetics_knock down_promote hsa-mir-29b-1 Leukemia, Myeloid, Acute 20628397 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 miR-29b1:The tumour-suppressive miR-29a/b1 cluster is regulated by CEBPA and blocked in human AML genetics_knock down_promote hsa-mir-125b-1 Leukemia-Lymphoma, Precursor B-Cell Lymphoblastic 16151463 disease of cellular proliferation DOID:7061 C83.5 D015452 an insertion of pre-miRNA into the immunoglobulin heavy-chain locus genetics_knock down_promote hsa-mir-101 Lung Neoplasms 25428391 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 particle can induce the secretion of interleukin-1β. Interleukin-1β subsequently induces the downregulation of mir-101, which may result in the upregulated level of EZH2, and occurrence of lung cancer. We for the first time proposed the role interleukin-1β-mir-101-EZH2 axes in the particle-induced lung cancer. Further study may be needed to decipher the detailed mechanism involved. genetics_knock down_promote hsa-mir-101-1 Lung Neoplasms 21849855 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-101 DNA Copy Loss is a Prominent Subtype Specific Event in Lung Cancer. genetics_knock down_promote hsa-mir-101-2 Lung Neoplasms 21849855 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-101 DNA Copy Loss is a Prominent Subtype Specific Event in Lung Cancer. genetics_knock down_promote hsa-mir-125b-1 Lung Neoplasms 14973191 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 deletion genetics_knock down_promote hsa-mir-301a Lung Neoplasms 20470754 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-301:blocking of miR-301 in A549 cells leads to a decrease in the expression of the host gene, ska2 genetics_knock down_promote hsa-mir-15a Lymphoma 16166262 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 the deletion or downregulation of mir-15a results in increased expression of BCL2. genetics_knock down_promote hsa-mir-16-1 Lymphoma 16166262 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 the deletion or downregulation of mir-15a results in increased expression of BCL2. genetics_knock down_promote hsa-mir-377 Lymphoma 25889255 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 Our results suggest that miR-377 is an important negative regulator of E2F and MAP3K7/NF-kB signaling pathway in melanoma cells; it is tempting to speculate that its silencing in melanoma promotes the tumorigenic and metastatic potential of the cells through activation of these pathways. genetics_knock down_promote hsa-mir-155 Lymphoma, B-Cell 25829072 disease of cellular proliferation DOID:707 D016393 109565 HP:0012191 A deficiency of miR-155 in the immune system causes attenuated immune functions. Clinically, several types of malignancy including diffuse large B-cell lymphoma have high miR-155 expression levels. genetics_knock down_promote hsa-mir-15a Lymphoma, Mantle-Cell 17940623 C83.10 D020522 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-16-1 Lymphoma, Mantle-Cell 17940623 C83.10 D020522 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-135a-1 Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion genetics_knock down_promote hsa-mir-135a-2 Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion or amplification genetics_knock down_promote hsa-mir-135b Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion or amplification genetics_knock down_promote hsa-mir-186 Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion genetics_knock down_promote hsa-mir-33b Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion, amplification or a mutation at the precursor miRNA genetics_knock down_promote hsa-mir-512-2 Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion. Antisense-based knockdown of miR-512-5p (mature sequence of miR-512-2) resulted in significant upregulation of MYCC expression in HeLa and A549 cells, while forced overexpression of miR-512-2 in medulloblastoma/PNET cell lines DAOY, UW-228-2, PFSK resulted in downregulation of MYCC protein. genetics_knock down_promote hsa-mir-548d-1 Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion genetics_knock down_promote hsa-mir-548d-2 Medulloblastoma 21793975 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 deletion genetics_knock down_promote hsa-let-7g Melanoma 22551973 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 The downregulation of this miRNA was associated with selective genomic loss in SSM cell lines and primary tumors. genetics_knock down_promote hsa-mir-155 Melanoma 25143000 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Our current study showed that both B16-F10 melanoma and Lewis lung carcinoma tumors grew much faster in bic/miR-155 knockout (miR-155(-/-) ) mice genetics_knock down_promote hsa-mir-200a Melanoma 22956368 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Loss of microRNA-200a and c, and microRNA-203 expression at the invasive front of primary cutaneous melanoma is associated with increased thickness and disease progression. genetics_knock down_promote hsa-mir-200c Melanoma 22956368 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Loss of microRNA-200a and c, and microRNA-203 expression at the invasive front of primary cutaneous melanoma is associated with increased thickness and disease progression. genetics_knock down_promote hsa-mir-203 Melanoma 22956368 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Loss of microRNA-200a and c, and microRNA-203 expression at the invasive front of primary cutaneous melanoma is associated with increased thickness and disease progression. genetics_knock down_promote hsa-mir-205 Melanoma 22525428 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Loss of microRNA-205 expression is associated with melanoma progression. genetics_knock down_promote hsa-mir-31 Mesothelioma 20463022 disease of cellular proliferation DOID:1790 C45.9 C562839 156240 HP:0100001 miR-31:Pro-tumorigenic effects of miR-31 loss in mesothelioma genetics_knock down_promote hsa-mir-15a Multiple Myeloma 17940623 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-16-1 Multiple Myeloma 17940623 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-29a Muscular Dystrophy, Duchenne 22434133 musculoskeletal system disease DOID:11723 G71.0 D020388 310200 Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis. genetics_knock down_promote hsa-mir-29b-1 Muscular Dystrophy, Duchenne 22434133 musculoskeletal system disease DOID:11723 G71.0 D020388 310200 Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis. genetics_knock down_promote hsa-mir-29b-2 Muscular Dystrophy, Duchenne 22434133 musculoskeletal system disease DOID:11723 G71.0 D020388 310200 Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis. genetics_knock down_promote hsa-mir-29c Muscular Dystrophy, Duchenne 22434133 musculoskeletal system disease DOID:11723 G71.0 D020388 310200 Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis. genetics_knock down_promote hsa-mir-17 Musculoskeletal Abnormalities [unspecific] 21892160 D009139 Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans. genetics_knock down_promote hsa-mir-18a Musculoskeletal Abnormalities [unspecific] 21892160 D009139 Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans. genetics_knock down_promote hsa-mir-19a Musculoskeletal Abnormalities [unspecific] 21892160 D009139 Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans. genetics_knock down_promote hsa-mir-19b-1 Musculoskeletal Abnormalities [unspecific] 21892160 D009139 Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans. genetics_knock down_promote hsa-mir-20a Musculoskeletal Abnormalities [unspecific] 21892160 D009139 Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans. genetics_knock down_promote hsa-mir-92a-1 Musculoskeletal Abnormalities [unspecific] 21892160 D009139 Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans. genetics_knock down_promote hsa-mir-155 Mycobacterium tuberculosis Infection 25846955 A18 D014376 607948 Following infection, miR-155-deficient C57BL/6 mice died significantly earlier and had significantly higher numbers of CFU in lungs than wild-type mice. genetics_knock down_promote hsa-mir-145 Myelodysplastic Syndromes 21873545 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 miR-145 affects megakaryocyte and erythroid differentiation.Patients with del(5q) MDS have decreased expression of miR-145 and increased expression of Fli-1. Combined loss of miR-145 and RPS14 cooperate to alter erythroid-megakaryocytic differentiation in a manner similar to the 5q- syndrome. genetics_knock down_promote hsa-mir-150 Myocardial Infarction 25824147 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 we show that genetic deletion of miR-150 in mice causes abnormalities in cardiac structural and functional remodelling after MI. genetics_knock down_promote hsa-mir-1-1 Myotonic Muscular Dystrophy 21685920 G71.11 D009223 160900 As a consequence of miR-1 loss, expression of GJA1 (connexin 43) and CACNA1C (Cav1.2), which are targets of miR-1, is increased in both DM1- and DM2-affected hearts. genetics_knock down_promote hsa-mir-1-2 Myotonic Muscular Dystrophy 21685920 G71.11 D009223 160900 As a consequence of miR-1 loss, expression of GJA1 (connexin 43) and CACNA1C (Cav1.2), which are targets of miR-1, is increased in both DM1- and DM2-affected hearts. genetics_knock down_promote hsa-mir-101-1 Neoplasms [unspecific] 19008416 C80.1 D009369 miR-101: Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer genetics_knock down_promote hsa-mir-101-2 Neoplasms [unspecific] 19008416 C80.1 D009369 miR-101: Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer genetics_knock down_promote hsa-mir-10a Neoplasms [unspecific] 24204315 C80.1 D009369 Loss of miR-10a activates lpo and collaborates with activated Wnt signaling in inducing intestinal neoplasia in female mice. genetics_knock down_promote hsa-mir-143 Neoplasms [unspecific] 20439436 C80.1 D009369 miR-143:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_knock down_promote hsa-mir-145 Neoplasms [unspecific] 20439436 C80.1 D009369 miR-145:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_knock down_promote hsa-mir-26a Neoplasms [unspecific] 25668004 C80.1 D009369 Loss of tumour-suppressive miR-26a/b enhanced cancer cell migration and invasion in OSCC through direct regulation of TMEM184B. Our data describing pathways regulated by tumour-suppressive miR-26a/b provide new insights into the potential mechanisms of OSCC oncogenesis and metastasis. genetics_knock down_promote hsa-mir-26b Neoplasms [unspecific] 25668004 C80.1 D009369 Loss of tumour-suppressive miR-26a/b enhanced cancer cell migration and invasion in OSCC through direct regulation of TMEM184B. Our data describing pathways regulated by tumour-suppressive miR-26a/b provide new insights into the potential mechanisms of OSCC oncogenesis and metastasis. genetics_knock down_promote hsa-mir-31 Neoplasms [unspecific] 20179198 C80.1 D009369 miR-31 is associated with defects in the p53 pathway and functions in serous ovarian cancer and other cancers genetics_knock down_promote hsa-mir-34a Neoplasms [unspecific] 18834855 C80.1 D009369 miR-34a: reduced or lost genetics_knock down_promote hsa-mir-150 Obesity 26833392 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 miR-150KO mice displayed exacerbated obesity-associated tissue inflammation and systemic insulin resistance genetics_knock down_promote hsa-mir-34a Obesity 27377585 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 miR-34a(-/-) mice are susceptible to diet-induced obesity. genetics_knock down_promote hsa-mir-132 Osteosarcoma 23801049 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Loss of microRNA-132 predicts poor prognosis in patients with primary osteosarcoma. genetics_knock down_promote hsa-mir-125b-1 Ovarian Neoplasms 14973191 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 deletion genetics_knock down_promote hsa-mir-145 Ovarian Neoplasms 22285623 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The loss of miR-145 can result in the activation of factors that promote oncogenesis and cellular pluripotency which in turn could lead to the development of ovarian cancer. genetics_knock down_promote hsa-mir-16-1 Ovarian Neoplasms 17012848 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Later on, deletion of mir-16-1 and mir-15a deletion were also identified in epithelial tumors, such as pituitary adenomas, ovarian and breast cancer. genetics_knock down_promote hsa-mir-31 Ovarian Neoplasms 20179198 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 miR-31 is associated with defects in the p53 pathway and functions in serous ovarian cancer and other cancers genetics_knock down_promote hsa-mir-101-1 Pancreatic Neoplasms 21932133 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Loss of MicroRNA-101 Promotes Overexpression of Histone Methyltransferase EZH2. genetics_knock down_promote hsa-mir-101-2 Pancreatic Neoplasms 21932133 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Loss of MicroRNA-101 Promotes Overexpression of Histone Methyltransferase EZH2. genetics_knock down_promote hsa-mir-126 Pancreatic Neoplasms 22845403 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Loss of miR-126 is crucial to pancreatic cancer progression. genetics_knock down_promote hsa-mir-214 Parkinson Disease 26349993 nervous system disease DOID:14330 G20 D010300 PS168600 The loss of miR-214 in PD resulted in the increase of α-synuclein expression, which was the potential mechanism underlying the neuroprotective effects of Resveratrol. genetics_knock down_promote hsa-mir-15a Pituitary Neoplasms 16885332 disease of cellular proliferation DOID:1785 C75.1 D010911 HP:0040277 a type of benign tumors displaying deletions at 13q14.3 and reduced expression of miR-16-1 and miR-15a genetics_knock down_promote hsa-mir-16-1 Pituitary Neoplasms 16885332 disease of cellular proliferation DOID:1785 C75.1 D010911 HP:0040277 a type of benign tumors displaying deletions at 13q14.3 and reduced expression of miR-16-1 and miR-15a genetics_knock down_promote hsa-mir-16-1 Pituitary Neoplasms 17012848 disease of cellular proliferation DOID:1785 C75.1 D010911 HP:0040277 Later on, deletion of mir-16-1 and mir-15a deletion were also identified in epithelial tumors, such as pituitary adenomas, ovarian and breast cancer. genetics_knock down_promote hsa-mir-142 Primary Immunodeficiency Disease 25931583 immune system disease DOID:612 D84.9 D007153 242850 miR-142 as an essential regulator of lymphopoiesis, and suggest that lesions in this miRNA gene may lead to primary immunodeficiency. genetics_knock down_promote hsa-mir-132 Progressive Supranuclear Palsy 21807765 nervous system disease DOID:678 G23.1 D013494 601104 MicroRNA-132 loss is associated with tau exon 10 inclusion in Supranuclear Palsy, Progressive. genetics_knock down_promote hsa-let-7 Prostate Neoplasms 23977098 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 MSCs co-evolve with prostate cancer cells in the tumor microenvironment, and the downregulation of let-7 by cancer-associated MSCs upregulates IL-6 expression. genetics_knock down_promote hsa-let-7c Prostate Neoplasms 22479342 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 MicroRNA let-7c Is Downregulated in Prostate Cancer and Suppresses Prostate Cancer Growth. genetics_knock down_promote hsa-mir-1 Prostate Neoplasms 25802280 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Our data support the existence of an AR-miR-1-SRC regulatory network.We propose that loss of miR-1 is one mechanistic link between low canonical Androgen receptor (AR) output and SRC-promoted metastatic phenotypes. genetics_knock down_promote hsa-mir-100 Prostate Neoplasms 24805183 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Loss of miR-100 enhances migration, invasion, epithelial-mesenchymal transition and stemness properties in prostate cancer cells through targeting Argonaute 2. genetics_knock down_promote hsa-mir-126 Prostate Neoplasms 24350576 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 These findings suggest for the first time that the loss of miR-126 expression may play a positive role in the malignant progression of PCa. genetics_knock down_promote hsa-mir-145 Prostate Neoplasms 27465939 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 ASC-derived conditioned medium (CM) significantly inhibited PC3M-luc2 cell proliferation, inducing apoptosis, but the effect was canceled by miR-145 knockdown in ASCs. genetics_knock down_promote hsa-mir-15a Prostate Neoplasms 17940623 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-15a Prostate Neoplasms 21472816 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The miR-15a-miR-16-1 locus is homozygously deleted in a subset of prostate cancers. genetics_knock down_promote hsa-mir-16-1 Prostate Neoplasms 17940623 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells. genetics_knock down_promote hsa-mir-16-1 Prostate Neoplasms 21472816 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The miR-15a-miR-16-1 locus is homozygously deleted in a subset of prostate cancers. genetics_knock down_promote hsa-mir-203 Prostate Neoplasms 24980827 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Loss of tumor suppressor mir-203 mediates overexpression of LIM and SH3 Protein 1 (LASP1) in high-risk prostate cancer thereby increasing cell proliferation and migration. genetics_knock down_promote hsa-mir-204 Prostate Neoplasms 25630658 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 not only tumor suppressor micro-RNA loss, but also significant genome rearrangement-driven regulatory loop perturbations play a role in the advanced cancer progression, conferring better pro-survival and metastatic potential. genetics_knock down_promote hsa-mir-205 Prostate Neoplasms 26059417 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Loss of tumor-suppressive microRNA-205 seems to enhance cancer cell migration and invasion in prostate cancer through direct regulation of centromere protein F. Our data describing pathways regulated by tumor-suppressive microRNA-205 provide new insights into the potential mechanisms of prostate cancer oncogenesis and metastasis. genetics_knock down_promote hsa-mir-34a Prostate Neoplasms 25436980 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 the bone metastasis and anti-apoptotic effects found in Ras signaling-activated prostate cancer cells require miR-34a deficiency, which in turn aids in cell survival by activating the WNT and anti-apoptotic signaling pathways thereby inducing TCF7 and BIRC5 expressions. genetics_knock down_promote hsa-mir-378 Prostate Neoplasms 25153390 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Loss of miR-378 in prostate cancer, a common regulator of KLK2 and KLK4, correlates with aggressive disease phenotype and predicts the short-term relapse of the patients. genetics_knock down_promote hsa-mir-122 Pterygium 27415790 nervous system disease DOID:0002116 H11.0 D011625 178200 Decreased expression of miR-122 in pterygium might result in abnormal cell apoptosis via its regulation of the expression of Bcl-w, and subsequently contribute to the development of pterygium. genetics_knock down_promote hsa-mir-21 Pulmonary Hypertension 24732886 cardiovascular system disease DOID:6432 I27.20 D006976 PS178600 HP:0002092 In vivo, genetic deletion of microRNA-21 in mice (miR-21(-/-) mice) resulted in functional activation of the PDCD4/caspase-3 axis in the pulmonary tissues, leading to the onset of progressive PH. genetics_knock down_promote hsa-mir-196a Renal Fibrosis 26940097 urinary system disease DOID:0050855 N26.9 HP:0030760 depletion of renal miR-196a/b by miR-196a/b antagomirs substantially aggravated UUO-induced renal fibrosis. genetics_knock down_promote hsa-mir-196b Renal Fibrosis 26940097 urinary system disease DOID:0050855 N26.9 HP:0030760 depletion of renal miR-196a/b by miR-196a/b antagomirs substantially aggravated UUO-induced renal fibrosis. genetics_knock down_promote hsa-mir-206 Rhabdomyosarcoma 27277678 disease of cellular proliferation DOID:3247 M62.82 D012208 268220 HP:0002859 Genetic deletion of miR-206 in a mouse model of FN-RMS accelerated and exacerbated tumor development genetics_knock down_promote hsa-mir-27a Rheumatoid Arthritis 27498552 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 However, miR-27a inhibition promoted the migration and invasion of FLS. genetics_knock down_promote hsa-mir-34a Rheumatoid Arthritis 22161761 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Downregulation of microRNA-34a* in rheumatoid arthritis synovial fibroblasts promotes apoptosis resistance. genetics_knock down_promote hsa-mir-126a Sepsis 26968021 A41.9 D018805 HP:0100806 The down-regulation of miR-126a-3p in endothelial cells resulted in the increased apoptosis, and decreased proliferation and migration, genetics_knock down_promote hsa-mir-150 Sepsis 26743170 A41.9 D018805 HP:0100806 miR-150(-/-) mice died rapidly after sepsis. genetics_knock down_promote hsa-mir-223 Sepsis 24486439 A41.9 D018805 HP:0100806 Taken together, these data indicate that loss of miR-223/-223* causes an aggravation of sepsis-induced inflammation, myocardial dysfunction and mortality. genetics_knock down_promote hsa-mir-200b Squamous Cell Carcinoma, Esophageal 27496804 disease of cellular proliferation DOID:3748 C562729 Correlating with the frequent loss of miR-200b in ESCC, both CDK2 and PAF levels are significantly increased in ESCC tumors compared to case-matched normal tissues. genetics_knock down_promote hsa-mir-451a Squamous Cell Carcinoma, Laryngeal or Hypopharyngeal 24918822 disease of cellular proliferation DOID:2876 Loss of tumour suppressive miR-451a enhanced cancer cell migration and invasion in HSCC through direct regulation of ESDN. Our miRNA signature and functional analysis of targets regulated by tumour suppressive miR-451a provide new insights into the potential mechanisms of HSCC oncogenesis and metastasis. genetics_knock down_promote hsa-mir-200a Squamous Cell Carcinoma, Oral 29480379 disease of cellular proliferation DOID:0050866 lack of significant alterations in miR-31 and miR-200a levels in saliva of OLP patients may be indicative for absence of malignant transformation genetics_knock down_promote hsa-mir-31 Squamous Cell Carcinoma, Oral 29480379 disease of cellular proliferation DOID:0050866 lack of significant alterations in miR-31 and miR-200a levels in saliva of OLP patients may be indicative for absence of malignant transformation genetics_knock down_promote hsa-mir-144 Thyroid Neoplasms 22049245 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 miR-199b-5p and miR-144 which were essentially lost in the carcinomas. genetics_knock down_promote hsa-mir-199b Thyroid Neoplasms 22049245 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 miR-199b-5p and miR-144 which were essentially lost in the carcinomas. genetics_knock down_promote hsa-mir-107 Urinary Bladder Cancer 21388952 urinary system disease DOID:11054 C67 D001749 109800 Specific deletion of p53 in urothelial cells is associated with specific overexpression of miR-18a and miR-19a and down-regulation of miR-107. genetics_knock down_promote hsa-mir-125b-1 Urinary Bladder Cancer 14973191 urinary system disease DOID:11054 C67 D001749 109800 deletion genetics_knock down_promote hsa-mir-181b-2 Urinary Bladder Cancer 17470785 urinary system disease DOID:11054 C67 D001749 109800 mir-181b-2 and mir-199b are 3.3 Mb from the peak of the colon Scc2 locus on Chr 2; homologous human miRNAs are located inside a cancer-associated genomic region, which is a region commonly deleted in bladder cancer. genetics_knock down_promote hsa-mir-199b Urinary Bladder Cancer 17470785 urinary system disease DOID:11054 C67 D001749 109800 mir-181b-2 and mir-199b are 3.3 Mb from the peak of the colon Scc2 locus on Chr 2; homologous human miRNAs are located inside a cancer-associated genomic region, which is a region commonly deleted in bladder cancer. genetics_knock down_promote hsa-mir-218-1 Urinary Bladder Cancer 21519788 urinary system disease DOID:11054 C67 D001749 109800 miR-218 on the genomic loss region of chromosome 4p15.31 functions as a tumor suppressor in bladder cancer. genetics_knock down_promote hsa-mir-218-2 Urinary Bladder Cancer 21519788 urinary system disease DOID:11054 C67 D001749 109800 miR-218 on the genomic loss region of chromosome 4p15.31 functions as a tumor suppressor in bladder cancer. genetics_knock down_suppress hsa-mir-155 Acute Lung Injury 27371731 S27 D055371 miR-155 gene inactivation protected mice from LPS-induced ALI genetics_knock down_suppress hsa-mir-155 Acute Myocardial Infarction 26589288 cardiovascular system disease DOID:9408 I21 D056989 608446 HP:0001658 We reveal that in vivo, miR-155 knockout improves left ventricular function, reduces infarct size, and attenuates collagen deposition, whereas overexpression of miR-155 produces the opposite effects. genetics_knock down_suppress hsa-mir-372 Adenocarcinoma, Gastric 26151747 disease of cellular proliferation DOID:3717 D37.1 D013274 Subcutaneously delivered LNAs reduce tumor growth of AGS xenografts in mice, upon formation of a stable, specific heteroduplex with the targeted miR-372 and -373 and LATS2 upregulation. genetics_knock down_suppress hsa-mir-18a Adenocarcinoma, Lung 27412935 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 Downregulation of miR-18a or miR-328 can inhibit the invasion and migration abilities of A549 cells effectively. genetics_knock down_suppress hsa-mir-192 Adenocarcinoma, Lung 26550150 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 MiR-192 inhibitor treated tumor exhibits sensitivity to cisplatin and gemcitabine therapy. genetics_knock down_suppress hsa-mir-214 Adenocarcinoma, Lung 26299367 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 downregulation of miR-214 expression in CSLCs resulted in a significant decrease in spheroid formation and the expression of the stem-cell markers Nanog, Oct-4, and Sox-2. genetics_knock down_suppress hsa-mir-328 Adenocarcinoma, Lung 27412935 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 Downregulation of miR-18a or miR-328 can inhibit the invasion and migration abilities of A549 cells effectively. genetics_knock down_suppress hsa-mir-184 Adenocarcinoma, Pancreatic Ductal 26722418 disease of cellular proliferation DOID:3498 C25.3 D021441 260350 The transfection of inhibitor effectively suppressed the expression of miR-184, and further inhibited both cell proliferation and invasion abilities, in addition to the up-regulation of pro-apoptotic protein caspase 3 expression. genetics_knock down_suppress hsa-mir-125b Amyotrophic Lateral Sclerosis 26794445 nervous system disease DOID:332 G12.21 D000690 PS105400 HP:0007354 by restoring A20 levels, miR-125b inhibition then sustains motor neuron survival. genetics_knock down_suppress hsa-mir-126 Asthma 19843690 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 Selective blockade of microRNA (miR)-126 suppressed the asthmatic phenotype genetics_knock down_suppress hsa-mir-21 Asthma 27448447 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. genetics_knock down_suppress hsa-mir-145 Atherosclerosis 25008143 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Absence of miR-143/145 significantly reduced atherosclerotic plaque size and macrophage infiltration. genetics_knock down_suppress hsa-mir-96 Bladder Neoplasms 26582573 C67 D001749 109800 HP:0009725 the inhibition of miR-96 expression remarkably decreased cell proliferation and promoted cell apoptosis of BC cell lines genetics_knock down_suppress hsa-mir-200a Breast Neoplasms 27433802 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 We further showed that inhibition of miR-200a function, mimicking the effect of calorie restriction on this microRNA, inhibited proliferation in both rat (LA7) and human (MCF7) luminal mammary cancer cell lines. genetics_knock down_suppress hsa-mir-21 Breast Neoplasms 21219636 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 In vitro assays showed that ERBB2 is a direct target of miR-125a-5p, which potently suppressed the proliferation of gastric cancer cells genetics_knock down_suppress hsa-mir-214 Breast Neoplasms 27328731 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Depleting miR-214 or elevating miR-148b blocked the dissemination of melanoma or breast cancer cells, an effect that could be accentuated by dual alteration. genetics_knock down_suppress hsa-mir-106b Carcinoma, Breast 27519168 D05 D001943 114480 HP:0003002 down-regulation of miR-106b increased the expression of FUT6 and resulted in an obvious decrease of cell migration, invasion, and proliferation in MDA-MB-231 cells. genetics_knock down_suppress hsa-mir-29a Carcinoma, Breast 29021023 D05 D001943 114480 HP:0003002 Knockdown of microRNA-29a Changes the Expression of Heat Shock Proteins in Breast Carcinoma MCF-7 Cells. genetics_knock down_suppress hsa-mir-29a Carcinoma, Breast 29435304 D05 D001943 114480 HP:0003002 Knockdown of microRNA-29a regulates the expression of apoptosis-related genes in MCF-7 breast carcinoma cells genetics_knock down_suppress hsa-mir-322 Carcinoma, Breast 28404630 D05 D001943 114480 HP:0003002 miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy. genetics_knock down_suppress hsa-mir-424 Carcinoma, Breast 28404630 D05 D001943 114480 HP:0003002 miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy. genetics_knock down_suppress hsa-mir-503 Carcinoma, Breast 28404630 D05 D001943 114480 HP:0003002 miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy. genetics_knock down_suppress hsa-mir-182 Carcinoma, Breast, Triple Negative 27476169 D064726 Knockdown of miR-182 promotes apoptosis via regulating RIP1 deubiquitination in TNF-伪-treated triple-negative breast cancer cells. genetics_knock down_suppress hsa-mir-9 Carcinoma, Breast, Triple Negative 27402080 D064726 miR-9 and miR-200 promoted and inhibited, respectively, the formation of vascular-like structures in vitro genetics_knock down_suppress hsa-mir-155 Carcinoma, Cervical 27470551 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 Moreover, knockdown of miR-155 was demonstrated to inhibit cell proliferation, migration, and invasion in vitro. genetics_knock down_suppress hsa-mir-181a Carcinoma, Cervical 27534652 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 Inhibition of microRNA-181a may suppress proliferation and invasion and promote apoptosis of cervical cancer cells through the PTEN/Akt/FOXO1 pathway. genetics_knock down_suppress hsa-mir-19b Carcinoma, Embryonal 25483911 disease of cellular proliferation DOID:3308 D018236 HP:0002898 The results demonstrated that miR鈥?9b knockdown inhibited the proliferation and apoptosis of P19 cells. genetics_knock down_suppress hsa-mir-503 Carcinoma, Esophageal 26580839 disease of cellular proliferation DOID:1107 C15.9 D004938 133239 HP:0011459 The specific inhibition of miR-503 expression remarkably suppressed proliferation and invasion of tumor cells. genetics_knock down_suppress hsa-mir-126 Carcinoma, Hepatocellular 27499630 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Inhibition of miR-126 expression increased Spred1 expression and decreased vascular endothelial growth factor expression (P<0.01). genetics_knock down_suppress hsa-mir-130b Carcinoma, Hepatocellular 26861561 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 knockdown or overexpression of miR-130b inhibited and promoted proliferation and metastasis of HCC cells genetics_knock down_suppress hsa-mir-150 Carcinoma, Hepatocellular 19617899 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 repressed in a subset of primary tumorscharacterized by poor prognosis; loss of miR-122 expression correlates with suppression of the hepatic phenotype and gain of metastatic properties; a diagnostic and prognostic marker genetics_knock down_suppress hsa-mir-181a Carcinoma, Hepatocellular 27384977 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Exogenous miR-181a expression in HepG2 cells reduced apoptosis, whereas inhibition of miR-181a in Hpe3B cells increased apoptosis. genetics_knock down_suppress hsa-mir-221 Carcinoma, Hepatocellular 22009537 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-221 silencing blocks hepatocellular carcinoma and promotes survival. genetics_knock down_suppress hsa-mir-221 Carcinoma, Hepatocellular 24993451 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Bioinformatics analysis identifies miR-221 as a core regulator in hepatocellular carcinoma and its silencing suppresses tumor properties. genetics_knock down_suppress hsa-mir-20a Carcinoma, Lung, Non-Small-Cell 26356817 C34.90 D002289 HP:0030358 Stable knock down of miR-20a increases T尾RII expression and inhibits tumorigenicity of lung cancer cells in vivo. genetics_knock down_suppress hsa-mir-27b Carcinoma, Lung, Non-Small-Cell 27221512 C34.90 D002289 HP:0030358 introduction of miR鈥?7b inhibitors significantly induced apoptosis and inhibited the proliferation of A549 cells. genetics_knock down_suppress hsa-mir-454 Carcinoma, Lung, Non-Small-Cell 27261580 C34.90 D002289 HP:0030358 Down-regulation of miR-454 could significantly reduce NSCLC cell proliferation, enhance cell apoptosis, and impair cell invasion and migration in vitro, while up-regulation of miR-454 showed opposite effects. genetics_knock down_suppress hsa-mir-21 Carcinoma, Lung, Non-Small-Cell 24804226 C34.90 D002289 HP:0030358 Silencing miR-21 sensitizes non-small cell lung cancer A549 cells to ionizing radiation through inhibition of PI3K/Akt. genetics_knock down_suppress hsa-mir-23b Carcinoma, Nasopharyngeal 27150436 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 inhibition of miR鈥?3b could significantly suppress NPC cell proliferation, migration and invasion. genetics_knock down_suppress hsa-mir-346 Carcinoma, Nasopharyngeal 27501413 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Inhibition of miR-346 significantly attenuated the migration and invasion of NPC cells. genetics_knock down_suppress hsa-mir-106a Carcinoma, Ovarian 27510094 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Downregulation of the expression of miR-106a inhibited cell growth and metastasis of ovarian cancer cells. genetics_knock down_suppress hsa-let-7i Carcinoma, Renal Cell 22926558 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 We also validated the prognostic value of miRNA let-7i in RCC. miR-138, located in chromosome 3p deletion, was also found to have suppressive effects on tumor proliferation and migration abilities. genetics_knock down_suppress hsa-mir-106b Carcinoma, Renal Cell 26648244 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Downregulation of miR-106b with a synthesized inhibitor suppressed cell migration and proliferation and induced renal cancer cell apoptosis genetics_knock down_suppress hsa-mir-138-1 Carcinoma, Renal Cell 22926558 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 We also validated the prognostic value of miRNA let-7i in RCC. miR-138, located in chromosome 3p deletion, was also found to have suppressive effects on tumor proliferation and migration abilities. genetics_knock down_suppress hsa-mir-138-2 Carcinoma, Renal Cell 22926558 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 We also validated the prognostic value of miRNA let-7i in RCC. miR-138, located in chromosome 3p deletion, was also found to have suppressive effects on tumor proliferation and migration abilities. genetics_knock down_suppress hsa-mir-183 Carcinoma, Thyroid, Medullary 22024754 disease of cellular proliferation DOID:3973 C73 C536914 155240 HP:0002865 MiR-183 knockdown in an MTC cell line (TT cells) reduced cellular proliferation in association with elevated LC3B expression. genetics_knock down_suppress hsa-mir-146b Carcinoma, Thyroid, Papillary 26883911 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 miR-146b-5p positively regulates migration and invasion of thyroid normal and tumor follicular cells genetics_knock down_suppress hsa-mir-221 Carotid Artery Diseases 19150885 G45.1 D002340 147820 HP:0005344 miR-221: knockdown of miR-221 and miR-222 in rat carotid arteries suppressed VSMC proliferation in vivo and neointimal lesion formation after angioplasty. The results indicate that miR-221 and miR-222 are novel regulators for VSMC proliferation and neointimal hype genetics_knock down_suppress hsa-mir-222 Carotid Artery Diseases 19150885 G45.1 D002340 147820 HP:0005344 miR-222: knockdown of miR-221 and miR-222 in rat carotid arteries suppressed VSMC proliferation in vivo and neointimal lesion formation after angioplasty. The results indicate that miR-221 and miR-222 are novel regulators for VSMC proliferation and neointimal hype genetics_knock down_suppress hsa-mir-224 Cerebral Ischemia 27165196 cardiovascular system disease DOID:2316 I67.82 D002545 HP:0002637 miR-224 inhibitor reduced neuronal cell apoptosis genetics_knock down_suppress hsa-mir-93 Cervical Neoplasms 27279231 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 Enforced miR-93 knockdown or RAB11FIP1 overexpression suppressed proliferation and promoted apoptosis genetics_knock down_suppress hsa-mir-21 Cholangiocarcinoma 25769721 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 anti-miR-21 treatment reduced liver tumor growth and prevented tumor development. genetics_knock down_suppress hsa-mir-34a Cholangiocarcinoma 26923637 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 The inhibition of miR-34a decreased proliferation, migration and invasion in cholangiocarcinoma cells. genetics_knock down_suppress hsa-mir-25 Choriocarcinoma 27120728 disease of cellular proliferation DOID:3594 C58 D002822 HP:0100768 Inhibition of miR-25 by its sponge in AGS cells resulted in suppressed cell viability (P<0.01) and promoted cell apoptosis (P<0.01) genetics_knock down_suppress hsa-mir-1-2 Chronic Heart Failure 17397913 cardiovascular system disease DOID:6000 I50 D006333 HP:0001635 deletion genetics_knock down_suppress hsa-mir-21 Colitis 29608690 gastrointestinal system disease DOID:0060180 K52.9 D003092 191390 HP:0002583 Loss of microRNA-21 Influences the Gut Microbiota Causing Reduced Susceptibility in a Murine Model of Colitis genetics_knock down_suppress hsa-let-7a-1 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7a-2 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7a-3 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7b Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7c Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7d Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7e Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7f-1 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7f-2 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7g Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7i Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-mir-21 Colorectal Adenocarcinoma 27364574 disease of cellular proliferation DOID:0050861 C19 C000599423 114500 Locked nucleic acid anti-miR-21 inhibits cell growth and invasive behaviors of a colorectal adenocarcinoma cell line genetics_knock down_suppress hsa-mir-15b Colorectal Carcinoma 26743779 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Inhibition of miR-15b activity by adenovirus carrying antimiR-15b sequence significantly increased MTSS1 and Klotho protein expression and subsequently decreased colony formation ability, invasion, and migration of HCT116 cells in vitro and liver metastasis of HCT116 tumors in vivo. genetics_knock down_suppress hsa-mir-21 Colorectal Carcinoma 25994220 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-21-knockout mice showed reduced expression of proinflammatory and procarcinogenic cytokines (interleukin (IL) 6, IL-23, IL-17A and IL-21) and a decrease in the size and number of tumours compared with the control mouse group. genetics_knock down_suppress hsa-mir-27a Colorectal Carcinoma 28423356 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Knockdown of miR-27a sensitizes colorectal cancer stem cells to TRAIL by promoting the formation of Apaf-1-caspase-9 complex. genetics_knock down_suppress hsa-mir-544a Colorectal Carcinoma 27165435 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-544a inhibitor and/or HOXA10 overexpression reduced lung metastases in HCT116 xenografts. genetics_knock down_suppress hsa-mir-592 Colorectal Carcinoma 27167185 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-592 inhibitor exhibited a significant reduction of migration, proliferation, and clonogenicity in CRC cells. genetics_knock down_suppress hsa-mir-195 Diabetic Cardiomyopathies 25994075 D058065 Therapeutic silencing of miR-195 reduces myocardial hypertrophy and improves coronary blood flow and myocardial function in diabetes genetics_knock down_suppress hsa-mir-155 Encephalomyelitis 24648472 nervous system disease DOID:640 B01.11 D004679 MiR-155 (-/-) mice are highly resistant to experimental autoimmune encephalomyelitis (EAE) genetics_knock down_suppress hsa-mir-223 Encephalomyelitis 26783338 nervous system disease DOID:640 B01.11 D004679 We demonstrate that miR-223-knockout mice display significantly reduced active and adoptive-transfer experimental autoimmune encephalomyelitis genetics_knock down_suppress hsa-mir-10b Endometrial Neoplasms 27447302 reproductive system disease DOID:1380 C54.1 D016889 608089 The silence of miR-10b resulted in significantly enhanced cell apoptosis, and remarkably reduced cell proliferation, migration, and invasion (p鈥?鈥?.05). genetics_knock down_suppress hsa-mir-210 Epilepsy 27471387 nervous system disease DOID:1826 G40 D004827 PS601068 HP:0001250 Our data showed that morphological changes of hippocampal neurons and apoptosis triggered by epilepsy were mitigated by miR-210 inhibition. genetics_knock down_suppress hsa-mir-21 Esophageal Neoplasms 27188433 C15.9 D004938 133239 HP:0100751 the proliferation, migration, and invasion of TE11 cells were less active in Inhibition-miR21 group. genetics_knock down_suppress hsa-mir-21 Fatty Liver, Non-Alcoholic 26338827 disease of metabolism DOID:0080208 K75.81 D065626 613282 MicroRNA-21 inhibition or suppression decreases liver injury, inflammation and fibrosis genetics_knock down_suppress hsa-mir-193 Gastric Neoplasms 26753960 disease of cellular proliferation DOID:10534 C16 D013274 137215 In AGS and MKN-45 cells, miR-193-3p downregulation reduced cancer proliferation, migration and 5-FU chemoresistance in vitro, and tumorigenicity in vivo. genetics_knock down_suppress hsa-mir-224 Gastric Neoplasms 27315344 disease of cellular proliferation DOID:10534 C16 D013274 137215 inhibition of miR-224 significantly reduced the expression of mTOR and improved caspase-9/3 expression while decreased cyclin D1/2 levels, attenuating gastric cancer cell proliferation. genetics_knock down_suppress hsa-mir-154 Glioblastoma 27338789 D005909 HP:0100843 Knockdown of miR-154 remarkably suppressed proliferation and migration of CD133(+) GBM cells. genetics_knock down_suppress hsa-mir-21 Glioblastoma 23732394 D005909 HP:0100843 Silencing of miR-21 by locked nucleic acid-lipid nanocapsule complexes sensitize human glioblastoma cells to radiation-induced cell death. genetics_knock down_suppress hsa-mir-21 Glioblastoma 25991676 D005909 HP:0100843 Both MPS1 and miR-21 depletion suppressed GBM cell proliferation genetics_knock down_suppress hsa-mir-21 Glioma 23077620 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Silencing of microRNA-21 confers radio-sensitivity through inhibition of the PI3K/AKT pathway and enhancing autophagy in malignant glioma cell lines genetics_knock down_suppress hsa-mir-155 Graft-Versus-Host Disease 27296836 D89.813 D006086 614395 miR-155-/- mice showed resistance to cardiac rejection along with weakened T-cell-mediated inflammation genetics_knock down_suppress hsa-mir-17 Graft-Versus-Host Disease 26138686 D89.813 D006086 614395 Furthermore, we evaluated a translational approach and found that systemic administration of antagomir to block miR-17 or miR-19b in this cluster significantly inhibited alloreactive T-cell expansion and interferon-纬 (IFN纬) production, and prolonged genetics_knock down_suppress hsa-mir-19b Graft-Versus-Host Disease 26138686 D89.813 D006086 614395 systemic administration of antagomir to block miR-17 or miR-19b in this cluster significantly inhibited alloreactive T-cell expansion and interferon-纬 (IFN纬) production genetics_knock down_suppress hsa-let-7c Heart Failure 25505600 I50 D006331 HP:0001635 Let-7c inhibitor prevented the deterioration of cardiac function postinfarction, as demonstrated by preserved LV ejection fraction and elevated cardiac output. genetics_knock down_suppress hsa-mir-21 Heart Failure 22923342 I50 D006331 HP:0001635 Atrial miR-21 knockdown suppresses atrial fibrosis and AF promotion, implicating miR-21 as an important signaling molecule for the AF substrate and pointing to miR-21 as a potential target for molecular interventions designed to prevent AF genetics_knock down_suppress hsa-mir-21 Heart Failure 24551276 I50 D006331 HP:0001635 After injection of miR-21 antagonist, the the cardiac atrophy and cardiac fibrosis were conspicuously ameliorated. genetics_knock down_suppress hsa-mir-122 Hepatitis C Virus Infection 22898980 disease by infectious agent DOID:1883 B19.2 D006526 609532 The use of an HSP90 inhibitor or knockdown of HSP90 decreased GW182 and miR-122 expression and significantly reduced HCV replication. genetics_knock down_suppress hsa-mir-122 Hepatitis C Virus Infection 25848473 disease by infectious agent DOID:1883 B19.2 D006526 609532 miR-122 promotes HCV accumulation, inhibition of miR-122 has been shown as an effective therapy for the treatment of HCV infection in both chimpanzees and humans. genetics_knock down_suppress hsa-mir-18a Immune System Disease [unspecific] 24131405 immune system disease DOID:2914 D89.9 D007154 Treatment of cells with a microRNA-18a mimic in PCPS (PCPS/miR-18) knocked down 90% expression of the microRNA-18a target gene ATM. genetics_knock down_suppress hsa-mir-155 Infection [unspecific] 28804270 D007239 Knockdown of miR-155 protects microglia against LPS-induced inflammatory injury via targeting RACK1: a novel research for intracranial infection genetics_knock down_suppress hsa-mir-138 Intervertebral Disc Degeneration 27207584 musculoskeletal system disease DOID:90 M51 D055959 603932 HP:0008419 inhibition of miR-138-5p downregulated PTEN protein expression and promoted activation of PI3K/AKT, and knockdown of either SIRT1 or the PI3K/Akt inhibitor (LY294002) abolished the effect of miR-138-5p on NP cell apoptosis. genetics_knock down_suppress hsa-mir-21 Ischemia-Reperfusion Injury 23681145 D015427 Knockdown of miR-21 induced significant up-regulation of programmed cell death protein 4 and phosphatase and tensin homolog deleted on chromosome 10, two proapoptotic target effectors of miR-21, and resulted in significant down-regulation of phosphorylated protein kinase B and increased tubular cell apoptosis. genetics_knock down_suppress hsa-mir-21 Ischemia-Reperfusion Injury 27030384 D015427 With downregulation of miR-21, the protection of delayed IPC was attenuated and PHD2 protein was increased. genetics_knock down_suppress hsa-mir-181a Ischemic Diseases [unspecific] 26283227 D007511 601367 Delivery of anti-miR-181a, which neutralizes endogenous miR-181a, significantly attenuated H2O2-induced decrease of HKII expression and disruption of mitochondrial membrane potential, improving the survival of MSCs exposed to H2O2. genetics_knock down_suppress hsa-mir-942 Kaposi Sarcoma 27440900 disease of cellular proliferation DOID:8632 C46 D012514 Suppression of miR-942-5p relieved I魏B伪 expression and reduced Vpr inhibition of KSHV replication, while overexpression of miR-942-5p enhanced Vpr inhibition of KSHV replication. genetics_knock down_suppress hsa-mir-150 Leukemia 23079661 C95 D007938 613065 HP:0001909 Blockade of miR-150 maturation by MLL-fusion/MYC/LIN-28 is required for MLL-associated leukemia genetics_knock down_suppress hsa-mir-21 Leukemia, Lymphoblastic, Acute 25451263 disease of cellular proliferation DOID:9952 C91.0 D054198 247640 HP:0006721 Transient inhibition of miR-21 resulted in increased apoptosis, PTEN upregulation and AKT dephosphorylation, whereas ectopic overexpression of miR-21 further conferred imatinib resistance. genetics_knock down_suppress hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 20129242 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 miR-15a and miR-16-1 were the first microRNAs linked to cancer because their genes are commonly deleted in human chronic lymphocytic leukemia (CLL) genetics_knock down_suppress hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 19744129 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Their aberrant expression has been associated with solid tumors and hematopoietic malignancies as suggested by the frequent deletion of mir-15a and mir-16-1 in chronic lymphocytic leukemia, the increased levels of mir-155 in diffuse large B-cell lymphomas and the increased levels of mir-181 in acute myeloid leukemia M1 and M2. genetics_knock down_suppress hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 19744129 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Their aberrant expression has been associated with solid tumors and hematopoietic malignancies as suggested by the frequent deletion of mir-15a and mir-16-1 in chronic lymphocytic leukemia, the increased levels of mir-155 in diffuse large B-cell lymphomas and the increased levels of mir-181 in acute myeloid leukemia M1 and M2. genetics_knock down_suppress hsa-mir-17 Leukemia, Lymphocytic, Chronic, B-Cell 25339346 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 In-vitro administration of antagomiR17 effectively reduced miR-17 expression and the proliferation of CLL-like MEC-1 cells. genetics_knock down_suppress hsa-mir-196b Leukemia, Myeloid, Acute 24334453 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Therapeutic inhibition of microRNA-21 and microRNA-196b inhibited in vitro leukemic colony forming activity and depleted in vivo leukemia-initiating cell activity of HOX-based leukemias, which led to leukemia-free survival in a murine AML model and delayed disease onset in xenograft models. genetics_knock down_suppress hsa-mir-21 Leukemia, Myeloid, Acute 24334453 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Therapeutic inhibition of microRNA-21 and microRNA-196b inhibited in vitro leukemic colony forming activity and depleted in vivo leukemia-initiating cell activity of HOX-based leukemias, which led to leukemia-free survival in a murine AML model and delayed disease onset in xenograft models. genetics_knock down_suppress hsa-mir-125b Leukemia, Myeloid, Chronic 27158338 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 inhibition of miR-125b decreased the proliferation rates and promoted apoptosis with cell cycle arrest at the G0/G1 phase in both K562 and NB-4 cells genetics_knock down_suppress hsa-mir-17 Leukemia, Myeloid, Chronic 25647305 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 Furthermore, overexpression of c-Myc or miR-17/20a alleviated NC induced differentiation and apoptosis in K562 cells. genetics_knock down_suppress hsa-mir-20a Leukemia, Myeloid, Chronic 25647305 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 Furthermore, overexpression of c-Myc or miR-17/20a alleviated NC induced differentiation and apoptosis in K562 cells. genetics_knock down_suppress hsa-mir-451 Leukemia, Myeloid, Chronic 27158338 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 inhibition of miR-125b decreased the proliferation rates and promoted apoptosis with cell cycle arrest at the G0/G1 phase in both K562 and NB-4 cells genetics_knock down_suppress hsa-mir-223 Leukemia, Promyelocytic, Acute 16325577 disease of cellular proliferation DOID:0060318 C92.4 D015473 612376 HP:0004836 In line with this, both RNAi against NFI-A and ectopic expression of miR-223 in acute promyelocytic leukemia (APL) cells enhance differentiation, whereas miR-223 knockdown inhibits the differentiation response to RA. genetics_knock down_suppress hsa-mir-92a Leukemia, Promyelocytic, Acute 24385779 disease of cellular proliferation DOID:0060318 C92.4 D015473 612376 HP:0004836 Down-regulation of miR-92a in APL cell line (HL-60) by LNA antagomir extensively decreased cell viability in APL. genetics_knock down_suppress hsa-mir-92a Leukemia, Promyelocytic, Acute 24627869 disease of cellular proliferation DOID:0060318 C92.4 D015473 612376 HP:0004836 The assessment of the apoptosis and necrosis indicates that miR-92a inhibition can decrease the viable HL-60 cells and this is at least partially due to induction of apoptosis. genetics_knock down_suppress hsa-mir-181b-1 Leukemia-Lymphoma, Precursor T-Cell Lymphoblastic 22916024 disease of cellular proliferation DOID:5599 C83.5 D054218 Deletion of mir-181a-1/b-1 expression inhibits the development of Notch1 oncogene-induced T cell acute lymphoblastic leukemia (T-ALL). mir-181a-1/b-1 controls the strength and threshold of Notch activity in tumorigenesis in part by dampening multiple negative feedback regulators downstream of NOTCH and pre-T cell receptor (TCR) signaling pathways. genetics_knock down_suppress hsa-mir-146a Listeriosis 29587465 disease by infectious agent DOID:11573 A32 D008088 MicroRNA-146a Deficiency Protects against Listeria monocytogenes Infection by Modulating the Gut Microbiota genetics_knock down_suppress hsa-mir-21 Liver Cirrhosis 27226339 endocrine system disease DOID:5082 K74 D008103 215600 HP:0001394 Ad-TuD-21 administered to liver fibrosis rats could remarkably suppress profibrotic gene expression genetics_knock down_suppress hsa-mir-21 Liver Cirrhosis 27775690 endocrine system disease DOID:5082 K74 D008103 215600 HP:0001394 Knockout of microRNA-21 reduces biliary hyperplasia and liver fibrosis in cholestatic bile duct ligated mice. genetics_knock down_suppress hsa-mir-214 Liver Fibrosis 26122702 K74 D008103 Pdgf-c Tg mice treated with LNA-antimiR-214 showed a marked reduction in fibrosis and tumor incidence compared with saline or LNA-miR-control-injected control mice. genetics_knock down_suppress hsa-mir-150 Liver Injury 26196694 S36.11 D056486 miR-150 deficiency prevents Fas-induced hepatocyte apoptosis and liver injury through regulation of the Akt pathway. genetics_knock down_suppress hsa-mir-192 Liver Injury 27129188 S36.11 D056486 Functional experiments confirmed a protective effect of down-regulation of miR-192-5p in hepatocytes, suggesting a role of miR-192-5p in limiting liver injury. genetics_knock down_suppress hsa-let-7a-1 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7a-2 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7a-3 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7b Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7c Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7d Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7e Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7f-1 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7f-2 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7g Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-let-7i Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers. genetics_knock down_suppress hsa-mir-21 Lung Neoplasms 25065740 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 PHF8 promotes miR-21 expression in human lung cancer, and miR-21 knockdown blocks the effects of PHF8 on proliferation and apoptosis of lung cancer cells. genetics_knock down_suppress hsa-mir-17 Lymphoma 27498867 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 Loss of miR-17鈭?2 in Myc(+) tumor cells leads to a global decrease in tumor cell metabolism, affecting both glycolytic and mitochondrial metabolism, whereas increased miR-17鈭?2 expression is sufficient to drive increased nutrient usage by tumor cells. genetics_knock down_suppress hsa-mir-23a Macular Degeneration 27411920 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 Inhibition of the H2O2-induced miR-23a by antagomiR protected the RPE cells from the oxidative stress-induced cell death. genetics_knock down_suppress hsa-mir-17 Medulloblastoma 24145352 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 Silencing of the miR-17~92 cluster family inhibits medulloblastoma progression. genetics_knock down_suppress hsa-mir-17 Medulloblastoma 24928431 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 Remarkably, deletion of the miR-17鈭?2 cluster abolished the development of SHH-MB in Ptch1(+/-) mice. genetics_knock down_suppress hsa-mir-19a Medulloblastoma 24145352 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 Silencing of the miR-17~92 cluster family inhibits medulloblastoma progression. genetics_knock down_suppress hsa-mir-125b Melanoma 26968260 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 inhibition of miR-125b reduces migratory and invasive potentials without affecting cell proliferation in vitro. genetics_knock down_suppress hsa-mir-21 Melanoma 27533779 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 MiR-21 can promote the proliferation, migration, and inhibit the apoptosis of human melanoma A375 cells by inhibiting SPRY1, PDCD4, and PTEN via ERK/NF-kB signaling pathway. genetics_knock down_suppress hsa-mir-214 Melanoma 27328731 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Depleting miR-214 or elevating miR-148b blocked the dissemination of melanoma or breast cancer cells, an effect that could be accentuated by dual alteration. genetics_knock down_suppress hsa-mir-17 Multiple Sclerosis 24644282 nervous system disease DOID:2377 G35 D009103 PS126200 T cell-specific miR-17-92 deficiency reduced TH17 differentiation and ameliorated experimental autoimmune encephalomyelitis (EAE) symptoms. genetics_knock down_suppress hsa-mir-223 Multiple Sclerosis 27083389 nervous system disease DOID:2377 G35 D009103 PS126200 miR223 promotes EAE, probably through enhancing DC activation and subsequently the differentiation of naive T cells toward Th1 and Th17 effector cells. genetics_knock down_suppress hsa-mir-206 Mycobacterium tuberculosis Infection 27291149 A18 D014376 607948 Inhibition of miR-206 markedly suppressed inflammatory cytokine secretion genetics_knock down_suppress hsa-mir-10b Myocardial Infarction 19595696 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Knockdown of microRNA-181 by lentivirus decreases the arrhythmogenic effect of skeletal myoblast transplantation in rat with myocardial infarction. genetics_knock down_suppress hsa-mir-126 Myocardial Infarction 26782549 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 miR-126 is down-regulated in myocardial ischemia-reperfusion injury and that the inhibition of miR-126 may protect against myocardial cell apoptosis caused by ischemia-reperfusion. genetics_knock down_suppress hsa-mir-150 Myocardial Infarction 26109086 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 MicroRNA-150 deletion in mice protects kidney from myocardial infarction-induced acute kidney injury. genetics_knock down_suppress hsa-mir-208a Myocardial Infarction 25936493 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Overexpression of antagomir-208a and pretreatment with atorvastatin and valsartan in the AMI group significantly decreased the area of myocardial fibrosis induced by infarction. genetics_knock down_suppress hsa-mir-208a Myocardial Infarction 26688617 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Therapeutic inhibition of miR-208a decreased cardiac fibrosis, hypertrophy, and apoptosis and significantly improved cardiac function 28 days after MI. genetics_knock down_suppress hsa-mir-210 Myocardial Infarction 26807177 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Inhibition of miR-210 expression improved the survival and cardiac function of MI mice. genetics_knock down_suppress hsa-mir-31 Myocardial Infarction 25925791 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 miR-31 downregulation alleviated myocardial infarct size in vivo. genetics_knock down_suppress hsa-mir-34a Myocardial Infarction 26082557 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 locked nucleic acid-based anti-miR-34a treatment diminished post-MI miR-34a upregulation in adult hearts and significantly improved post-MI remodeling. genetics_knock down_suppress hsa-mir-128 Myocardial Ischemic-Reperfusion Injury 27150726 D015428 miR鈥?28 antagomirs significantly reduced apoptosis in hearts subjected to I/R injury genetics_knock down_suppress hsa-mir-21 Myocardial Ischemic-Reperfusion Injury 26862785 D015428 recombinant HMGB1鈥堿-box treatment protects against I/R injury and the mechanisms may involve inhibition of miR-21 expression. genetics_knock down_suppress hsa-mir-92a Myocardial Ischemic-Reperfusion Injury 24941323 D015428 Inhibiting miR-92a can attenuate myocardiocyte apoptosis induced by hypoxia/reoxygenation by targeting Smad7. genetics_knock down_suppress hsa-let-7 Neoplasms [unspecific] 26033159 C80.1 D009369 we found that expression of DICER1 hotspot mutants promoted cell proliferation, whereas wild-type (WT) DICER1 inhibited cell proliferation. Furthermore, targets of let-7 family miRNAs are enriched among the up-regulated genes, suggesting that loss of let-7 may be impacting downstream pathways. Our results reveal that DICER1 hotspot mutations are implicated in common malignancies and may constitute a unique oncogenic pathway. genetics_knock down_suppress hsa-let-7a-1 Neoplasms [unspecific] 20614490 C80.1 D009369 let-7a:Gastric carcinoma has relatively lower expression of let-7a genetics_knock down_suppress hsa-let-7a-2 Neoplasms [unspecific] 20614490 C80.1 D009369 let-7a:Gastric carcinoma has relatively lower expression of let-7a genetics_knock down_suppress hsa-let-7a-3 Neoplasms [unspecific] 20614490 C80.1 D009369 let-7a:Gastric carcinoma has relatively lower expression of let-7a genetics_knock down_suppress hsa-let-7b Neoplasms [unspecific] 25682900 C80.1 D009369 our findings suggest that let-7b contributes to the fidelity of cell division via regulation of Aurora B. Moreover, the loss of let-7b in aggressive tumors may drive tumorigenesis by up-regulation of Aurora B and other targets of the miRNA, which further supports the role of let-7b in tumor suppression. genetics_knock down_suppress hsa-let-7b Neoplasms [unspecific] 24423609 C80.1 D009369 Reduction of let-7a3/let-7b miRNA may be one of mechanisms leading to overexpression of HMGA2 in AT/RT tissues. genetics_knock down_suppress hsa-mir-143 Neoplasms [unspecific] 22330136 C80.1 D009369 Loss of microRNA-143/145 disturbs cellular growth and apoptosis of human epithelial cancers by impairing the MDM2-p53 feedback loop. genetics_knock down_suppress hsa-mir-145 Neoplasms [unspecific] 22330136 C80.1 D009369 Loss of microRNA-143/145 disturbs cellular growth and apoptosis of human epithelial cancers by impairing the MDM2-p53 feedback loop. genetics_knock down_suppress hsa-mir-155 Neoplasms [unspecific] 25598954 C80.1 D009369 the proper increase of miR-155 inhibitor concentration can inhibit miR-155 and consequently increase caspase-3 activity and induce apoptosis in the Jurkat cells leading to cell death ultimately. genetics_knock down_suppress hsa-mir-200a Neoplasms [unspecific] 20832727 C80.1 D009369 miR-200a:Loss of miR-200 inhibition of Suz12 leads to polycomb-mediated repression required for the formation and maintenance of cancer stem cells genetics_knock down_suppress hsa-mir-200b Neoplasms [unspecific] 20832727 C80.1 D009369 miR-200b:Loss of miR-200 inhibition of Suz12 leads to polycomb-mediated repression required for the formation and maintenance of cancer stem cells genetics_knock down_suppress hsa-mir-200c Neoplasms [unspecific] 20832727 C80.1 D009369 miR-200c:Loss of miR-200 inhibition of Suz12 leads to polycomb-mediated repression required for the formation and maintenance of cancer stem cells genetics_knock down_suppress hsa-mir-204 Neoplasms [unspecific] 23285024 C80.1 D009369 Genomic Loss of Tumor Suppressor miRNA-204 Promotes Cancer Cell Migration and Invasion by Activating AKT/mTOR/Rac1 Signaling and Actin Reorganization genetics_knock down_suppress hsa-mir-205 Neoplasms [unspecific] 26446417 C80.1 D009369 When HEC-50B cells and HEC-1-A cells were treated with anti-miR-205 inhibitor, the migration and invasion were decreased as compared with the negative control. genetics_knock down_suppress hsa-mir-21 Neoplasms [unspecific] 29540832 C80.1 D009369 miR-21 depletion in macrophages promotes tumoricidal polarization and enhances PD-1 immunotherapy genetics_knock down_suppress hsa-mir-222 Neoplasms [unspecific] 26909602 C80.1 D009369 Anti-miR-222 inhibitor treatment decreased cell proliferation, migration, tube formation, and induced apoptosis. genetics_knock down_suppress hsa-mir-210 Nervous System Diseases [unspecific] 26708520 C72.9 D009422 Application of miR-210 inhibitor efficiently downregulated endogenous miR-210, protected apoptosis and neurite retraction in bupivacaine damaged DRG neurons. genetics_knock down_suppress hsa-mir-124-1 Neuroblastoma 22024478 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Silencing of miR-124 induces neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis through promoting AHR. genetics_knock down_suppress hsa-mir-124-2 Neuroblastoma 22024478 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Silencing of miR-124 induces neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis through promoting AHR. genetics_knock down_suppress hsa-mir-124-3 Neuroblastoma 22024478 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Silencing of miR-124 induces neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis through promoting AHR. genetics_knock down_suppress hsa-mir-127 Obesity 27532680 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 On the other hand, locked nucleic acid inhibitor synthesized to target miR-127-5p significantly increased b-F1-ATPase translation efficiency in myotubes. genetics_knock down_suppress hsa-mir-21 Obesity 25141837 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 MiR-21 inhibition reduced body weight, as well as adipocyte size and serum triglycerides were significantly decreased. genetics_knock down_suppress hsa-mir-21 Osteosarcoma 27513462 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 microRNA-21 inhibition slowed proliferation and exogenously expressed microRNA-21 promoted this process. genetics_knock down_suppress hsa-mir-182 Ovarian Neoplasms 24825857 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 we found that anti-miR182 treatment can significantly reduce tumor burden (size), local invasion, and distant metastasis compared with its control in both models. genetics_knock down_suppress hsa-mir-630 Ovarian Neoplasms 26725326 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Treatment with the combination of anti-miR-630 and anti-vascular endothelial growth factor antibody in mice resulted in rescue of Dicer expression and significantly decreased tumor growth and metastasis. genetics_knock down_suppress hsa-mir-183 Pancreatic Adenocarcinoma 26870180 disease of cellular proliferation DOID:4074 C25.3 miR-183 knockdown decreased cell growth and motility in pancreatic cancer cells and significantly increased the expression of SOCS-6. genetics_knock down_suppress hsa-mir-199a Pancreatic Neoplasms 26918939 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Inhibition of miR-199a/-214 using hairpin inhibitors significantly inhibited TGF尾-induced differentiation markers (e.g. 伪-SMA, collagen, PDGF尾R), migration and proliferation. genetics_knock down_suppress hsa-mir-222 Pancreatic Neoplasms 26535064 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 we co-transfected miR-222 inhibitor and p57 si-RNA into Capan-2 cells, and found that proliferation-suppressing effects of miR-222 inhibitor on Capan-2 cells could be partially reversed by silencing p57. genetics_knock down_suppress hsa-mir-106b Pituitary Neoplasms 27465551 disease of cellular proliferation DOID:1785 C75.1 D010911 HP:0040277 Down-regulation of miR-106b or up-regulation of PTEN could suppress cell proliferation and invasion of AtT-20 cells, and PTEN expression plasmid could partially simulate the function of miR-106b. genetics_knock down_suppress hsa-mir-18a Prostate Neoplasms 24752237 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Interestingly, miR-18a knockdown decreased cell growth in prostate cancer cells and significantly decreased prostate tumor growth in in vivo nude mice experiments through STK4-mediated dephosphorylation of AKT and thereby inducing apoptosis. genetics_knock down_suppress hsa-mir-9 Prostate Neoplasms 27447934 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Inhibition of miR-9 resulted in reduced migratory and invasive potential of the M12 cell line, and reduced tumour growth and metastases in male athymic nude mice. genetics_knock down_suppress hsa-mir-221 Rheumatoid Arthritis 25891943 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Downregulation of miR-221 significantly suppressed the expression of pro-inflammatory cytokines and the chemokine genetics_knock down_suppress hsa-mir-155 Spinal Cord Injuries 25651871 S34.139A D013119 Mir-155 deficiency suppresses Th17 cell differentiation and improves locomotor recovery after SCI. genetics_knock down_suppress hsa-mir-31 Squamous Cell Carcinoma, Esophageal 26286729 disease of cellular proliferation DOID:3748 C562729 anti-miR-31 reduced miR-31 overexpression (P = .002) and suppressed the esophageal preneoplasia in Zn-deficient rats. genetics_knock down_suppress hsa-mir-23a Squamous Cell Carcinoma, Head and Neck 24317043 disease of cellular proliferation DOID:5520 C76.0 C535575 Transfection with anti-miR-23a inhibited the proliferation of HN4 cells and induced cell apoptosis. genetics_knock down_suppress hsa-mir-24 Squamous Cell Carcinoma, Head and Neck 27513190 disease of cellular proliferation DOID:5520 C76.0 C535575 Inhibition of miR-24-3p reduced cell proliferation, colony formation efficiency and reversed chemoresistance in HNSCC cells. genetics_knock down_suppress hsa-mir-455 Squamous Cell Carcinoma, Oral 27235675 disease of cellular proliferation DOID:0050866 MiR-455-5p knockdown reduced both the anchorage-independent growth and the proliferative ability of oral cancer cells genetics_knock down_suppress hsa-mir-24 Squamous Cell Carcinoma, Tongue 27350307 disease of cellular proliferation DOID:0050865 C02.9 Inhibition of miR-24 significantly suppressed the proliferation, migration and invasion of TSCC cells in vitro. genetics_knock down_suppress hsa-mir-155 Stroke 26354913 I64 D020521 601367 HP:0001297 In Vivo Inhibition of miR-155 Promotes Recovery after Experimental Mouse Stroke. genetics_knock down_suppress hsa-mir-24-1 Tourette Syndrome 17462786 disease of mental health DOID:11119 F95.2 D005879 137580 A mutation in the 3'UTR of the SLITRK1 gene which is associated with Tourette's syndrome was found to enhance repression of the SLITRK mRNA by miR-189, presumably preventing SLITRK1's promotion of dendritic growth. genetics_knock down_suppress hsa-mir-21 Vascular Disease [unspecific] 25360215 cardiovascular system disease DOID:178 I72.9 D000783 Low expression of miR-21 significantly inhibited VSMC proliferation, invasion and migration. genetics_knock down_suppress hsa-mir-137 Vascular Injuries 27497953 D057772 Down-regulation of miR-137 ameliorates HG-induced injury in HUVECs by overexpression of AMPK伪1, leading to increasing cellular reductive reactions and decreasing oxidative stress. genetics_overexpression_promote hsa-mir-19a Acute Erythroid Leukemia 22451425 C94.0 D004915 overexpression of individual miRNAs from this locus, miR-19a or miR-92a, results in B-cell hyperplasia and erythroleukemia, respectively. genetics_overexpression_promote hsa-mir-92a Acute Erythroid Leukemia 22451425 C94.0 D004915 overexpression of individual miRNAs from this locus, miR-19a or miR-92a, results in B-cell hyperplasia and erythroleukemia, respectively. genetics_overexpression_promote hsa-mir-92a Acute Myocardial Infarction 27411964 cardiovascular system disease DOID:9408 I21 D056989 608446 HP:0001658 Further, it could be observed in cellular experiments that treatment of miR-92a mimics can further upregulate endothelial injury markers. genetics_overexpression_promote hsa-mir-449a Adenocarcinoma, Lung 23614048 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 Overexpression of miR-449a in CL1-0 cells effectively increased irradiation-induced DNA damage and apoptosis,altered the cell cycle distribution and eventually led to sensitization of CL1-0 to irradiation. genetics_overexpression_promote hsa-mir-212 Adenocarcinoma, Pancreatic Ductal 27814273 disease of cellular proliferation DOID:3498 C25.3 D021441 260350 Overexpressions of miR-212 are associated with poor prognosis of patients with pancreatic ductal adenocarcinoma. genetics_overexpression_promote hsa-mir-221 Adenocarcinoma, Pancreatic Ductal 27230035 disease of cellular proliferation DOID:3498 C25.3 D021441 260350 Overexpressing miR-221 significantly increased cell vitality and promoted cell proliferation and G1-to-S phase transition of the cell cycle in Capan-2 cells genetics_overexpression_promote hsa-mir-146a Alzheimer Disease 27241555 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 Overexpression of miRNA-146a in SH-SY5Y cells significantly decreased Lrp2 expression, resulting in a reduction of Akt activation and induction of proapoptotic caspase-3, thereby increasing cell apoptosis. genetics_overexpression_promote hsa-mir-206 Alzheimer Disease 27277332 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 miR鈥?06 upregulation enhanced LPS鈥慽nduced inflammation and A尾 release in microglia genetics_overexpression_promote hsa-mir-21 Asthma 26651881 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 This study provides the first in vitro evidence that overexpression of miR-21 in HASM cells can trigger cell proliferation and migration, and the effects of miR-21 depend on the level of PTEN. genetics_overexpression_promote hsa-mir-181a Atherosclerosis 27460740 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 The exogenous overexpression of miR-181a accelerates the apoptosis rates of HUVECs in response to H2O2. genetics_overexpression_promote hsa-mir-29a Atrial Fibrillation 27341015 cardiovascular system disease DOID:0060224 I48.0 D001281 PS608583 HP:0005110 miR-29a-3p transfection in cardiomyocytes produced the effects on the ICa genetics_overexpression_promote hsa-mir-222 Bladder Neoplasms 26800397 C67 D001749 109800 HP:0009725 Overexpression of miR-222 attenuated cisplatin-induced cell death in bladder cancer cells. genetics_overexpression_promote hsa-mir-92b Bladder Neoplasms 27430302 C67 D001749 109800 HP:0009725 In this study, we demonstrated that miR-92b could uniquely promote cell migration and invasion of BCa cells, but had no effect on cell proliferation. genetics_overexpression_promote hsa-mir-29c Brain Disease [unspecific] 25678279 nervous system disease DOID:936 G93.40 D001927 608033 over-expression of miR-29c effectively reduced Birc2 (also Bak1) mRNA and protein levels, increased infarct volume and apoptosis, and deteriorated neurological outcomes, whereas down-regulation played a neuroprotective role. genetics_overexpression_promote hsa-mir-141 Breast Neoplasms 27075851 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Ectopic expression of miR-141 in nonexpressing MDA-MB-231 enhanced brain metastatic colonization (5/9 mice vs 0/10 mice,P= .02). genetics_overexpression_promote hsa-mir-146a Breast Neoplasms 25123132 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Overexpression of miR-146a in basal-like breast cancer cells confers enhanced tumorigenic potential in association with altered p53 status. genetics_overexpression_promote hsa-mir-200c Breast Neoplasms 25329395 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Overexpression of microRNA-200c predicts poor outcome in patients with PR-negative breast cancer. genetics_overexpression_promote hsa-mir-21 Breast Neoplasms 21917003 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 High expression of miR-21 in tumor stroma correlates with increased cancer cell proliferation in human breast cancer. genetics_overexpression_promote hsa-mir-21 Breast Neoplasms 22547075 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 DNA damage induces NF-kB-dependent microRNA-21 upregulation and promotes breast cancer cell invasion. genetics_overexpression_promote hsa-mir-214 Breast Neoplasms 26951965 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the overexpression of miR鈥?14 markedly increased cell viability and abrogated the apoptosis triggered by serum starvation genetics_overexpression_promote hsa-mir-221 Breast Neoplasms 27044817 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Enforced expression of miR-221/222 promoted breast cancer cell proliferation, migration and invasion via targeting PTEN/Akt pathway. genetics_overexpression_promote hsa-mir-222 Breast Neoplasms 27044817 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Enforced expression of miR-221/222 promoted breast cancer cell proliferation, migration and invasion via targeting PTEN/Akt pathway. genetics_overexpression_promote hsa-mir-23b Breast Neoplasms 24966325 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Ectopic expression of the miRNAs in the weakly metastatic mouse 4TO7 mammary tumor cell line had no effect on proliferation or morphology of tumor cells in vitro but was found to increase lung metastasis in a mouse model of breast cancer metastasis. genetics_overexpression_promote hsa-mir-24 Breast Neoplasms 24966325 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Ectopic expression of the miRNAs in the weakly metastatic mouse 4TO7 mammary tumor cell line had no effect on proliferation or morphology of tumor cells in vitro but was found to increase lung metastasis in a mouse model of breast cancer metastasis. genetics_overexpression_promote hsa-mir-27b Breast Neoplasms 24966325 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Ectopic expression of the miRNAs in the weakly metastatic mouse 4TO7 mammary tumor cell line had no effect on proliferation or morphology of tumor cells in vitro but was found to increase lung metastasis in a mouse model of breast cancer metastasis. genetics_overexpression_promote hsa-mir-449a Breast Neoplasms 26934316 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 In vitro, miR-449a promoted breast cancer cell proliferation, clonogenic survival, migration, and invasion. genetics_overexpression_promote hsa-mir-183 Carcinoma, Breast 27476679 D05 D001943 114480 HP:0003002 Overexpression of miR-183-5p significantly enhanced the cell proliferation and inhibited cell apoptosis in MCF-7 and MDA-MB-231 cells. genetics_overexpression_promote hsa-mir-21 Carcinoma, Cervical 25963606 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 Overexpression of miR-21 promotes the proliferation and migration of cervical cancer cells via the inhibition of PTEN. genetics_overexpression_promote hsa-mir-21 Carcinoma, Cervical 26884851 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 The overexpression of HPV E7 protein facilitated the expression of miR-21, which potentiated Hela cell proliferation and invasion. genetics_overexpression_promote hsa-mir-1 Carcinoma, Colon 27511117 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 overexpression of PIK3CA-premir1 in HCT116 and SW480 cells resulted in significant reduction of the sub-G1 cell distribution and apoptotic cell rate and resulted in increased cell proliferation. genetics_overexpression_promote hsa-mir-125b Carcinoma, Gastric 27220320 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Overexpression of miR-125b promoted gastric cancer cell migration and invasion in vitro and metastasis in vivo. genetics_overexpression_promote hsa-mir-200c Carcinoma, Gastric 27498672 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Finally, ectopic expression of miR-200c or knockdown of DNMT3a expression impeded GC cell growth, migration and invasion. genetics_overexpression_promote hsa-mir-483 Carcinoma, Gastric 27511210 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 overexpression of miR鈥?83鈥?p by transfection with miR鈥?83鈥?p mimics significantly increased cell proliferation and Annexin V鈥憄ropidium iodide staining indicated the suppression of cell apoptosis. genetics_overexpression_promote hsa-mir-93 Carcinoma, Gastric 27021515 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 miR-93 promoted the development of gastric tumor growth in xenograft mice genetics_overexpression_promote hsa-let-7 Carcinoma, Hepatocellular 28796071 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of microRNA let-7 correlates with disease progression and poor prognosis in hepatocellular carcinoma genetics_overexpression_promote hsa-let-7a Carcinoma, Hepatocellular 28796071 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of microRNA let-7 correlates with disease progression and poor prognosis in hepatocellular carcinoma genetics_overexpression_promote hsa-let-7e Carcinoma, Hepatocellular 28796071 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of microRNA let-7 correlates with disease progression and poor prognosis in hepatocellular carcinoma genetics_overexpression_promote hsa-mir-106b Carcinoma, Hepatocellular 23483935 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Over-Expression of miR-106b Promotes Cell Migration and Metastasis in Hepatocellular Carcinoma by Activating Epithelial-Mesenchymal Transition Process genetics_overexpression_promote hsa-mir-122 Carcinoma, Hepatocellular 22140464 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-122 expression is highly elevated in quiescent human primary hepatocytes (hPHs) but lost or attenuated in hESCs and HCCs, while an opposing expression pattern is observed for Pkm2. Depleting hESCs and HCCs of Pkm2, or overexpressing miR-122, leads to a common deficiency in self-renewal and proliferation. genetics_overexpression_promote hsa-mir-1269 Carcinoma, Hepatocellular 25472505 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 overexpression of miR-1269 promotes cell proliferation in HCC through directly suppressing FOXO1, and functions as an oncomiR in HCC. genetics_overexpression_promote hsa-mir-153 Carcinoma, Hepatocellular 25714700 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Over-expression of miR-153 down-regulated the activity of Etoposide and Paclitaxel on cell cycle arrest of HepG2 cells and the effect of Sorafenib on the invasion and migration of HepG2 cells. genetics_overexpression_promote hsa-mir-155 Carcinoma, Hepatocellular 22071603 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Up-regulation of microRNA-155 promotes cancer cell invasion and predicts poor survival of hepatocellular carcinoma following liver transplantation. genetics_overexpression_promote hsa-mir-15b Carcinoma, Hepatocellular 27499071 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 It was observed that high expression of miR-15b promoted cell proliferation of the HCC cells, while low expression of miR-15b suppressed cell growth and induced the apoptosis of HepG2 cells. genetics_overexpression_promote hsa-mir-196a Carcinoma, Hepatocellular 27108614 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 HCV core protein increased the expression of miR鈥?96a, and that overexpression of miR鈥?96a in the HepG2 and Huh鈥? HCC cell lines promoted cell proliferation by inducing the G1鈥慡 transition. genetics_overexpression_promote hsa-mir-222 Carcinoma, Hepatocellular 24955159 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 MiR-222 overexpression induced an enhancement of HepG2 cell proliferation in vitro, paralleling with an altered cell cycle progression via increased cell population in S phase. genetics_overexpression_promote hsa-mir-522 Carcinoma, Hepatocellular 26960688 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-522 overexpression promoted cell proliferation, colony formation, and cell cycle progression, whereas knockdown of miR-522 reduced these effects. genetics_overexpression_promote hsa-mir-548a Carcinoma, Hepatocellular 27340352 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 overexpression of miR-548a-5p in HCC cell lines promoted cell proliferation, increased colony forming ability and hampered cell apoptosis. genetics_overexpression_promote hsa-mir-615 Carcinoma, Hepatocellular 22819824 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-615-5p is restrictedly expressed in cirrhotic and cancerous liver tissues and its overexpression alleviates the tumorigenic effects in hepatocellular carcinoma. genetics_overexpression_promote hsa-mir-92b Carcinoma, Hepatocellular 27100897 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-92b could promote cell proliferation and metastasis of HCC in vitro and in vivo. genetics_overexpression_promote hsa-mir-23a Carcinoma, Laryngeal 26171041 disease of cellular proliferation DOID:2600 C32.3 D007822 21198 HP:0012118 Ectopic expression of miR-23a and knockdown of APAF-1 significantly promoted cell proliferation and colony formation, and inhibited early apoptosis in Hep2 cells. genetics_overexpression_promote hsa-let-7g Carcinoma, Lung, Non-Small-Cell 18308936 C34.90 D002289 HP:0030358 we observed significant growth reduction of both murine and human non-small cell lung tumors when overexpression of let-7g was induced from lentiviral vectors genetics_overexpression_promote hsa-mir-221 Carcinoma, Lung, Non-Small-Cell 26131134 C34.90 D002289 HP:0030358 We found that miR-222 overexpression increased cell viability and proliferative rate in H460 cells while opposite effects were obtained by down-regulation of miR-222. genetics_overexpression_promote hsa-mir-92a Carcinoma, Lung, Non-Small-Cell 26432332 C34.90 D002289 HP:0030358 upregulation of miR-92a in NSCLC cells promoted cell proliferation, migration, and invasion, decreased apoptosis and caspase-3 activity, and enhanced chemoresistance of NSCLC cells, whereas downregulation of miR-92a showed the opposite effects. genetics_overexpression_promote hsa-mir-21 Carcinoma, Lung, Non-Small-Cell 22335905 C34.90 D002289 HP:0030358 Overexpression of miR-21 promotes proliferation and reduces apoptosis in non-small cell lung cancer]. genetics_overexpression_promote hsa-mir-141 Carcinoma, Nasopharyngeal 27010857 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 ectopic expression of miR-141 can significantly promote cell proliferation and inhibit apoptosis in NPC genetics_overexpression_promote hsa-mir-200a Carcinoma, Nasopharyngeal 26718506 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Overexpression of miR-200a resulted in the proliferation of CNE2 cells. genetics_overexpression_promote hsa-mir-205 Carcinoma, Nasopharyngeal 26880795 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Overexpression of miR-205 increased the proliferation, migration and invasion of CNE2 cells genetics_overexpression_promote hsa-mir-92a Carcinoma, Nasopharyngeal 27366095 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 miR-92a overexpression potentiated the migration and invasion of 6-10B cells genetics_overexpression_promote hsa-mir-194 Carcinoma, Ovarian 27486333 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Overexpression of miR-194 in ovarian cancer cells promotes cell proliferation, migration, and invasion; in contrast, inhibition of the expression of miR-194 has the opposite effects. genetics_overexpression_promote hsa-mir-196b Carcinoma, Ovarian 28387653 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Overexpression of microRNA-196b Accelerates Invasiveness of Cancer Cells in Recurrent Epithelial Ovarian Cancer Through Regulation of Homeobox A9. genetics_overexpression_promote hsa-mir-760 Carcinoma, Ovarian 27726922 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 MiR-760 overexpression promotes proliferation in ovarian cancer by downregulation of PHLPP2 expression. genetics_overexpression_promote hsa-mir-940 Carcinoma, Pancreatic 27459115 C25.3 C562463 260350 HP:0002894 Over-expression of microRNA-940 promotes cell proliferation by targeting GSK3尾 and sFRP1 in human pancreatic carcinoma. genetics_overexpression_promote hsa-mir-96 Carcinoma, Prostate 27164937 disease of cellular proliferation DOID:10286 D07.5 D011471 176807 HP:0012125 Overexpressing miR-96 led to increased proliferation and colony formation of normal prostate epithelial cells. genetics_overexpression_promote hsa-mir-100 Carcinoma, Renal Cell 23378187 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 miR-100 overexpression strongly associates with advanced tumor progression and unfavorable clinical outcome of patients with RCC genetics_overexpression_promote hsa-mir-222 Carcinoma, Thyroid, Papillary 23023232 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 The overexpression of oncogenic miR-221 and miR-222 caused by HMGB1 is associated with an increase in malignancy scores, namely cell growth and motility. genetics_overexpression_promote hsa-mir-214 Cardiomegaly 25085702 I51.7 D006332 HP:0001640 Cardiac hypertrophy and dysfunction induced by overexpression of miR-214 in vivo. genetics_overexpression_promote hsa-mir-206 Cardiomegaly 26333362 I51.7 D006332 HP:0001640 Cardiac-specific overexpression of miR-206 in mice induced hypertrophy and protected the heart from ischemia/reperfusion injury genetics_overexpression_promote hsa-mir-146a Cerebral Ischemia 27449900 cardiovascular system disease DOID:2316 I67.82 D002545 HP:0002637 In conclusion, our study revealed that miR-146a contributes to OGD/R injury in vitro. genetics_overexpression_promote hsa-mir-182 Cerebral Ischemia 27242323 cardiovascular system disease DOID:2316 I67.82 D002545 HP:0002637 miR-182 plays an aggressive role in the cerebral ischemia injury genetics_overexpression_promote hsa-mir-27b Cervical Neoplasms 26706910 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 Upregulation of miR-27b significantly accelerated the proliferation, cell cycle transition from G1 to S phase, migration and invasion of C33A cells genetics_overexpression_promote hsa-mir-27b Cervical Neoplasms 26910911 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 MiR-27b, up-regulated by E7, promoted CaSki and SiHa cell proliferation and invasion, inhibit paclitaxel-induced apoptosis. genetics_overexpression_promote hsa-mir-21 Cholesteatoma 27376830 integumentary system disease DOID:869 H71.9 D002781 604183 HP:0009797 miR-21 promotes the proliferation and invasion of cholesteatoma keratinocytes. genetics_overexpression_promote hsa-mir-21 Choriocarcinoma 27922982 disease of cellular proliferation DOID:3594 C58 D002822 HP:0100768 miR-21 Is Overexpressed in Hydatidiform Mole Tissues and Promotes Proliferation, Migration, and Invasion in Choriocarcinoma Cells. genetics_overexpression_promote hsa-mir-125a Chronic Hepatitis B 25993287 B18.0-.1 D019694 610424 Conversely, the overexpression of miR-125a or knockdown of A20 mimicked HBx to enhance TRAIL susceptibility in hepatocytes. genetics_overexpression_promote hsa-mir-146a Chronic Hepatitis B 26996068 B18.0-.1 D019694 610424 Overexpression of miR-146a reduced NK cell-mediated cytotoxicity genetics_overexpression_promote hsa-mir-17 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-17 Colon Neoplasms 22065543 D12.6 D003110 HP:0100273 MiR-17-92 cluster and its paralogs were significantly overexpressed in colon tumor. No significant associations were found between the deregulation of certain miRNAs and the clinical and pathologic characteristics observed in patients. Kaplan-Meier curves demonstrated significantly reduced overall survival in patients expressing high levels of miR-17. In multivariate Cox models, miR-17 overexpression (HR 2.67; P=0.007) and TNM staging (HR 8.87; P=0.002) were significantly associated with a risk of death. genetics_overexpression_promote hsa-mir-18a Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-18a Colon Neoplasms 22065543 D12.6 D003110 HP:0100273 MiR-17-92 cluster and its paralogs were significantly overexpressed in colon tumor. No significant associations were found between the deregulation of certain miRNAs and the clinical and pathologic characteristics observed in patients. Kaplan-Meier curves demonstrated significantly reduced overall survival in patients expressing high levels of miR-17. In multivariate Cox models, miR-17 overexpression (HR 2.67; P=0.007) and TNM staging (HR 8.87; P=0.002) were significantly associated with a risk of death. genetics_overexpression_promote hsa-mir-19a Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-19a Colon Neoplasms 22065543 D12.6 D003110 HP:0100273 MiR-17-92 cluster and its paralogs were significantly overexpressed in colon tumor. No significant associations were found between the deregulation of certain miRNAs and the clinical and pathologic characteristics observed in patients. Kaplan-Meier curves demonstrated significantly reduced overall survival in patients expressing high levels of miR-17. In multivariate Cox models, miR-17 overexpression (HR 2.67; P=0.007) and TNM staging (HR 8.87; P=0.002) were significantly associated with a risk of death. genetics_overexpression_promote hsa-mir-19b-1 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-19b-1 Colon Neoplasms 22065543 D12.6 D003110 HP:0100273 MiR-17-92 cluster and its paralogs were significantly overexpressed in colon tumor. No significant associations were found between the deregulation of certain miRNAs and the clinical and pathologic characteristics observed in patients. Kaplan-Meier curves demonstrated significantly reduced overall survival in patients expressing high levels of miR-17. In multivariate Cox models, miR-17 overexpression (HR 2.67; P=0.007) and TNM staging (HR 8.87; P=0.002) were significantly associated with a risk of death. genetics_overexpression_promote hsa-mir-20a Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-20a Colon Neoplasms 22065543 D12.6 D003110 HP:0100273 MiR-17-92 cluster and its paralogs were significantly overexpressed in colon tumor. No significant associations were found between the deregulation of certain miRNAs and the clinical and pathologic characteristics observed in patients. Kaplan-Meier curves demonstrated significantly reduced overall survival in patients expressing high levels of miR-17. In multivariate Cox models, miR-17 overexpression (HR 2.67; P=0.007) and TNM staging (HR 8.87; P=0.002) were significantly associated with a risk of death. genetics_overexpression_promote hsa-mir-92a-1 Colon Neoplasms 17965831 D12.6 D003110 HP:0100273 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-92a-1 Colon Neoplasms 22065543 D12.6 D003110 HP:0100273 MiR-17-92 cluster and its paralogs were significantly overexpressed in colon tumor. No significant associations were found between the deregulation of certain miRNAs and the clinical and pathologic characteristics observed in patients. Kaplan-Meier curves demonstrated significantly reduced overall survival in patients expressing high levels of miR-17. In multivariate Cox models, miR-17 overexpression (HR 2.67; P=0.007) and TNM staging (HR 8.87; P=0.002) were significantly associated with a risk of death. genetics_overexpression_promote hsa-mir-34a Colorectal Adenocarcinoma 28624481 disease of cellular proliferation DOID:0050861 C19 C000599423 114500 miR-34a overexpression predicts poor prognostic outcome in colorectal adenocarcinoma, independently of clinicopathological factors with established prognostic value. genetics_overexpression_promote hsa-mir-10b Colorectal Carcinoma 28345456 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Overexpression of miR-10b in colorectal cancer patients: Correlation with TWIST-1 and E-cadherin expression. genetics_overexpression_promote hsa-mir-183 Colorectal Carcinoma 26717041 disease of cellular proliferation DOID:0080199 C19 D015179 114500 over-expression of miR-183 resulted in the attenuation of rapamycin- or starvation-induced autophagy in cancer cells, whereas inhibition of endogenous miR-183 stimulated autophagy and apoptosis. genetics_overexpression_promote hsa-mir-194 Colorectal Carcinoma 29109785 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Overexpression of miR-194 Reverses HMGA2-driven Signatures in Colorectal Cancer. genetics_overexpression_promote hsa-mir-205 Colorectal Carcinoma 27271572 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-205 and miR-373 may differentially contribute to the aggressive phenotype of MAC in CRC. genetics_overexpression_promote hsa-mir-21 Colorectal Carcinoma 24149370 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-21 is a key player in oncogenic EMT, its overexpression is controlled by the cooperation of genetic and epigenetic alterations, and its levels, along with ITGβ4 and PDCD4 expression, could be exploited as a prognostic tool for CRC metastasis. genetics_overexpression_promote hsa-mir-223 Colorectal Carcinoma 25270282 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Overexpression of miR-223 correlates with tumor metastasis and poor prognosis in patients with colorectal cancer. genetics_overexpression_promote hsa-mir-32 Colorectal Carcinoma 24123284 disease of cellular proliferation DOID:0080199 C19 D015179 114500 MiR-32 overexpression was correlated with specific CRC clinicopathological features and may be a marker of poor prognosis in CRC patients. MiR-32 and PTEN expression were inversely correlated, and miR-32 may be associated with the development of CRC. genetics_overexpression_promote hsa-mir-373 Colorectal Carcinoma 27271572 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-205 and miR-373 may differentially contribute to the aggressive phenotype of MAC in CRC. genetics_overexpression_promote hsa-mir-410 Colorectal Carcinoma 27177325 disease of cellular proliferation DOID:0080199 C19 D015179 114500 overexpression of miR鈥?10 resulted in an increase in growth activity and decrease in the extent of apoptosis genetics_overexpression_promote hsa-mir-28 Colorectal Carcinoma 22240480 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-28-5p altered expression of CCND1 and HOXB3, whereas miR-28-3p bound NM23-H1. Overexpression of miR-28-5p reduced CRC cell proliferation, migration, and invasion in vitro, whereas miR-28-3p increased CRC cell migration and invasion in vitro. genetics_overexpression_promote hsa-mir-410 Colorectal Carcinoma 25272045 disease of cellular proliferation DOID:0080199 C19 D015179 114500 MiR-410 is overexpressed in liver and colorectal tumors and enhances tumor cell growth by silencing FHL1 via a direct/indirect mechanism. genetics_overexpression_promote hsa-mir-200b Cytotoxicity Tests, Immunologic 27183614 D003601 Cells overexpressing miR-200b/c or miR-217 showed reduced sensitivity to CDC genetics_overexpression_promote hsa-mir-200c Cytotoxicity Tests, Immunologic 27183614 D003601 Cells overexpressing miR-200b/c or miR-217 showed reduced sensitivity to CDC genetics_overexpression_promote hsa-mir-217 Cytotoxicity Tests, Immunologic 27183614 D003601 Cells overexpressing miR-200b/c or miR-217 showed reduced sensitivity to CDC genetics_overexpression_promote hsa-mir-375 Diabetes Mellitus 28017506 disease of metabolism DOID:9351 E10-E14 D003920 222100 HP:0000819 Insulin producing cells generation by overexpression of miR-375 in adipose-derived mesenchymal stem cells from diabetic patients. genetics_overexpression_promote hsa-mir-429 Diabetes Mellitus 27299781 disease of metabolism DOID:9351 E10-E14 D003920 222100 HP:0000819 increased miR-429 could down-regulate the expression of Ocln by targeting the Ocln 3'-UTR, which impaired intestinal barrier function in DM mice. genetics_overexpression_promote hsa-mir-132 Diabetes Mellitus, Type 2 26218441 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Overexpression of miR-132 or miR-212 enhances glucose and GLP-1-stimulated insulin secretion. genetics_overexpression_promote hsa-mir-212 Diabetes Mellitus, Type 2 26218441 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Overexpression of miR-132 or miR-212 enhances glucose and GLP-1-stimulated insulin secretion. genetics_overexpression_promote hsa-mir-144 Diabetic Cardiomyopathies 26164195 D058065 The miR-144 mimics aggravated high glucose-induced ROS formation and apoptosis in cardiomyocytes genetics_overexpression_promote hsa-mir-205 Endometrial Neoplasms 28105153 reproductive system disease DOID:1380 C54.1 D016889 608089 Overexpression of microRNA-205 predicts lymph node metastasis and indicates an unfavorable prognosis in endometrial cancer. genetics_overexpression_promote hsa-mir-302 Fanconi Anemia 26343459 hematopoietic system disease DOID:13636 D61.09 D005199 PS227650 Taken together, our results suggest that overexpression of miR-302 plays a critical role in the regulation of FANCD2 monoubiquitination, resulting in characteristic defects in DNA repair within cells. genetics_overexpression_promote hsa-mir-106a Gastric Neoplasms 27142596 disease of cellular proliferation DOID:10534 C16 D013274 137215 Abnormal over-expression of miR-106a significantly promoted gastric cancer cell proliferation, metastasis, inhibited the cell apoptosis. genetics_overexpression_promote hsa-mir-17 Gastric Neoplasms 25047501 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-17 in gastric cancer is correlated with proliferation-associated oncogene amplification. genetics_overexpression_promote hsa-mir-17 Gastric Neoplasms 23333058 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-17-5p/20a promoted gastric cancer cell cycle progression and inhibited cell apoptosis, whereas knockdown of miR-17-5p/20a resulted in cell cycle arrest and increased apoptosis. genetics_overexpression_promote hsa-mir-181b Gastric Neoplasms 27383203 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-181b mimic induced an in vitro EMT-like change to a phenotype similar to that following TGF-尾 treatment alone and was reversed by miRNA-181b inhibitor. genetics_overexpression_promote hsa-mir-20a Gastric Neoplasms 23333058 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-17-5p/20a promoted gastric cancer cell cycle progression and inhibited cell apoptosis, whereas knockdown of miR-17-5p/20a resulted in cell cycle arrest and increased apoptosis. genetics_overexpression_promote hsa-mir-20a Gastric Neoplasms 26286834 disease of cellular proliferation DOID:10534 C16 D013274 137215 ectopic expression of miR-20a dramatically decreased the expression of NFKBIB; increased the expression of p65, livin, and survivin genetics_overexpression_promote hsa-mir-21 Gastric Neoplasms 25230738 disease of cellular proliferation DOID:10534 C16 D013274 137215 This meta-analysis indicates that miR-21 detection has a prognostic value in patients with gastric cancer. In addition, overexpression of miR-21 is associated with worse tumor differentiation, lymph node metastasis, and TNM stage. genetics_overexpression_promote hsa-mir-222 Gastric Neoplasms 27323780 disease of cellular proliferation DOID:10534 C16 D013274 137215 Gastrin-induced miR-222 overexpression resulted in reduced expression and cytoplasmic mislocalisation of p27kip1, which in turn caused actin remodelling and increased migration in AGSGR cells. genetics_overexpression_promote hsa-mir-27a Gastric Neoplasms 27409164 disease of cellular proliferation DOID:10534 C16 D013274 137215 And overexpression of miR-27a-3p, but not miR-27a-5p, markedly promoted gastric cancer cell proliferation in vitro as well as tumor growth in vivo. genetics_overexpression_promote hsa-mir-340 Gastric Neoplasms 27374211 disease of cellular proliferation DOID:10534 C16 D013274 137215 Functionally, forced expression of miR-340 promoted cell viability, proliferation, colony formation and cell cycle progression in the SGC-7901 cells genetics_overexpression_promote hsa-mir-210 Gastrointestinal Stromal Tumor 24623741 disease of cellular proliferation DOID:9253 C49.A D046152 606764 Overexpression of miR-210 is associated with SDH-related pheochromocytomas, paragangliomas, and gastrointestinal stromal tumours. genetics_overexpression_promote hsa-mir-125b-2 Glioblastoma 21879257 D005909 HP:0100843 miR-125b-2 overexpression might confer glioblastoma stem cells resistance to TMZ. genetics_overexpression_promote hsa-mir-138 Glioblastoma 26887050 D005909 HP:0100843 Transient transfection of miR-138 mimics in glioma cells with low basal miR-138 expression increased glioma cell proliferation. genetics_overexpression_promote hsa-mir-223 Glioblastoma 28035389 D005909 HP:0100843 overexpression of miR-223 increases TMZ chemoresistance, while inhibition of miR-223 with antagomir markedly decreases TMZ chemoresistance in GBM cells genetics_overexpression_promote hsa-mir-26a Glioblastoma 20080666 D005909 HP:0100843 Overexpression of miR-26a in PTEN-competent and PTEN-deficient glioblastoma cells promoted tumor growth in vivo, and it further increased growth in cells overexpressing CDK4 or CENTG1. genetics_overexpression_promote hsa-mir-9 Glioblastoma 27036038 D005909 HP:0100843 hsa-miR-9 overexpression leads to MAPKAP signaling inhibition, partially by interfering with the MAPK14/MAPKAP3 complex. Further, hsa-miR-9 overexpression initiates re-arrangement of actin filament genetics_overexpression_promote hsa-mir-183 Glioma 26879754 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Introduction of miR-183 mimics into U251 cells could promoted, while its antisense oligos inhibited cell proliferation and invasion. genetics_overexpression_promote hsa-mir-19a Glioma 27329239 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Overexpression of miR-19a by a miR-19a mimic promoted glioma cell proliferation and invasion. genetics_overexpression_promote hsa-mir-215 Glioma 26317904 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 In summary, miR-215 is overexpressed in human glioma, is involved in TGF-β1-induced oncogenesis, and can be used as a marker of poor prognosis in glioma patients. genetics_overexpression_promote hsa-mir-363 Glioma 27495233 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Transfection of miR-363 induced cell survival, while inhibition of miR-363 significantly reduced glioma cell viability. genetics_overexpression_promote hsa-mir-96 Glioma 26846266 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 In vivo, microRNA-96 overexpression inhibits the apoptosis and increases tumor growth. genetics_overexpression_promote hsa-mir-29b Hearing Loss 27635430 H91.93 D034381 miR-29b overexpression induces cochlear hair cell apoptosis through the regulation of SIRT1/PGC-1α signaling: Implications for age-related hearing loss. genetics_overexpression_promote hsa-mir-132 Heart Failure 23011132 I50 D006331 HP:0001635 MiR-212/132 null mice are protected from pressure-overload-induced heart failure, whereas cardiomyocyte-specific overexpression of the miR-212/132 family leads to pathological cardiac hypertrophy, heart failure and death in mice. genetics_overexpression_promote hsa-mir-195 Heart Failure 25100012 I50 D006331 HP:0001635 Cardiac overexpression of miR-195 results in pathological cardiac growth and heart failure in transgenic mice. genetics_overexpression_promote hsa-mir-21 Heart Failure 26865549 I50 D006331 HP:0001635 Overexpression of miR-21 in this monocyte cell line activated a fibrotic gene programme and promoted monocyte-to-fibrocyte transition genetics_overexpression_promote hsa-mir-212 Heart Failure 23011132 I50 D006331 HP:0001635 MiR-212/132 null mice are protected from pressure-overload-induced heart failure, whereas cardiomyocyte-specific overexpression of the miR-212/132 family leads to pathological cardiac hypertrophy, heart failure and death in mice. genetics_overexpression_promote hsa-mir-22 Heart Failure 24086656 I50 D006331 HP:0001635 microRNA-22 promotes heart failure through coordinate suppression of PPAR/ERR-nuclear hormone receptor transcription. genetics_overexpression_promote hsa-mir-30c Heart Failure 24789369 I50 D006331 HP:0001635 Taken together these data indicate impaired mitochondrial function due to OXPHOS protein depletion as a potential cause for the observed dilated cardiomyopathic phenotype in miRNA-30c transgenic mice. genetics_overexpression_promote hsa-mir-17 Hematologic Neoplasms 17011485 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 The miR-17-92 cluster is amplified in hematopoietic malignancies. genetics_overexpression_promote hsa-mir-17 Hematologic Neoplasms 25597017 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 overexpression of miR-17-92 in a limited number of hematopoietic cells is sufficient to cause B cell malignancies. genetics_overexpression_promote hsa-mir-18a Hematologic Neoplasms 17011485 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 The miR-17-92 cluster is amplified in hematopoietic malignancies. genetics_overexpression_promote hsa-mir-19a Hematologic Neoplasms 17011485 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 The miR-17-92 cluster is amplified in hematopoietic malignancies. genetics_overexpression_promote hsa-mir-19b-1 Hematologic Neoplasms 17011485 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 The miR-17-92 cluster is amplified in hematopoietic malignancies. genetics_overexpression_promote hsa-mir-20a Hematologic Neoplasms 17011485 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 The miR-17-92 cluster is amplified in hematopoietic malignancies. genetics_overexpression_promote hsa-mir-449a Hepatitis B Virus Infection 27138288 disease by infectious agent DOID:2043 B16/18 D006509 610424 Ectopic miR-449a expression in HCC cells strongly enhanced HBV replication, transcription, progeny virions secretion, and antigen expression in a dose-dependent manner. genetics_overexpression_promote hsa-mir-155 Hepatitis C Virus Infection 21750860 disease by infectious agent DOID:1883 B19.2 D006526 609532 Coordinated increase of miRNA-155 and miRNA-196b expression correlates with the detection of the antigenomic strand of hepatitis C virus in peripheral blood mononuclear cells. genetics_overexpression_promote hsa-mir-196b Hepatitis C Virus Infection 21750860 disease by infectious agent DOID:1883 B19.2 D006526 609532 Coordinated increase of miRNA-155 and miRNA-196b expression correlates with the detection of the antigenomic strand of hepatitis C virus in peripheral blood mononuclear cells. genetics_overexpression_promote hsa-mir-21 Hypertrophic Scar 27207585 L91.0 D017439 overexpression of miR-21 promoted fibroproliferative expression in fibroblasts. genetics_overexpression_promote hsa-mir-146b Inflammation 23813877 D007249 MicroRNA-146b improves intestinal injury in mouse colitis by activating nuclear factor-κB and improving epithelial barrier function. genetics_overexpression_promote hsa-mir-221 Inflammation 23023232 D007249 The overexpression of oncogenic miR-221 and miR-222 caused by HMGB1 is associated with an increase in malignancy scores, namely cell growth and motility. genetics_overexpression_promote hsa-mir-221 Inflammation 26549234 D007249 Enforced expression of miR-221 significantly increased the production of proinflammatory cytokines genetics_overexpression_promote hsa-mir-9 Influenza 27322373 respiratory system disease DOID:8469 J09-J11 D007251 614680 Overexpression of miR-9 enhanced viral gene expression and production of infectious progeny genetics_overexpression_promote hsa-mir-125a Juvenile Rheumatoid Arthritis 27014994 musculoskeletal system disease DOID:676 M08.4 D001171 604302 miR-125a-5p overexpression enhanced M2b polarization and altered other polarized populations genetics_overexpression_promote hsa-mir-210 Kidney Neoplasms 26985942 disease of cellular proliferation DOID:263 C64 D007680 ACHN cell proliferation and invasion were significantly increased and apoptosis was significantly decreased (P < 0.05) when miR-210 was overexpressed. genetics_overexpression_promote hsa-mir-31 Leiomyosarcoma 19602040 C55 D007890 HP:0100243 overexpression; leads to HMGA2 overexpression; Disrupting the control of HMGA2 and let-7 pairs promotes ULMS cell growth in vitro. genetics_overexpression_promote hsa-mir-125b Leukemia 21118985 C95 D007938 613065 HP:0001909 Thus, we show that overexpression of miR-125b is sufficient both to shorten the latency of BCR-ABL-induced leukemia and to independently induce leukemia in a mouse model. genetics_overexpression_promote hsa-mir-17 Leukemia 22451425 C95 D007938 613065 HP:0001909 In both murine and human leukemias, p53 inactivation contributed to the selective overexpression of oncogenic miR-92a and miR-19a, and down-regulation of tumor-suppressive miR-17. genetics_overexpression_promote hsa-mir-17 Leukemia 24145403 C95 D007938 613065 HP:0001909 The miR-17∼92 overexpression was driven by the Eµ-enhancer and Ig heavy-chain promoter, and a 3' GFP tag was added to the transgene to track the miR expression. genetics_overexpression_promote hsa-mir-9 Leukemia 23798388 C95 D007938 613065 HP:0001909 miR-9 is an essential oncogenic microRNA specifically overexpressed in mixed lineage leukemia-rearranged leukemia. genetics_overexpression_promote hsa-mir-18a Leukemia, B-Cell 24145403 C91.31 D015448 151430 The miR-17∼92 overexpression was driven by the Eµ-enhancer and Ig heavy-chain promoter, and a 3' GFP tag was added to the transgene to track the miR expression. genetics_overexpression_promote hsa-mir-19a Leukemia, B-Cell 24145403 C91.31 D015448 151430 The miR-17∼92 overexpression was driven by the Eµ-enhancer and Ig heavy-chain promoter, and a 3' GFP tag was added to the transgene to track the miR expression. genetics_overexpression_promote hsa-mir-19b Leukemia, B-Cell 24145403 C91.31 D015448 151430 The miR-17∼92 overexpression was driven by the Eµ-enhancer and Ig heavy-chain promoter, and a 3' GFP tag was added to the transgene to track the miR expression. genetics_overexpression_promote hsa-mir-92a Leukemia, B-Cell 24145403 C91.31 D015448 151430 The miR-17∼92 overexpression was driven by the Eµ-enhancer and Ig heavy-chain promoter, and a 3' GFP tag was added to the transgene to track the miR expression. genetics_overexpression_promote hsa-mir-223 Leukemia, Lymphocytic, Chronic, B-Cell 22145958 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 microRNA-223 expression is uniformly down-regulated in B cell lymphoproliferative disorders and is associated with poor survival in chronic lymphocytic leukemia patients. genetics_overexpression_promote hsa-mir-125b Leukemia, Myeloid, Acute 22689670 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 We previously described a t(2;11)(p21;q23) chromosomal translocation found in patients with myelodysplasia or acute myeloid leukemia that leads to over-expression of the microRNA miR-125b, and we showed that transplantation of mice with murine stem/progenitor cells overexpressing miR-125b is able to induce leukemia. genetics_overexpression_promote hsa-mir-130a Leukemia, Myeloid, Acute 29493383 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 MiR-130a is aberrantly overexpressed in adult acute myeloid leukemia with t(8;21) and its suppression induces AML cell death. genetics_overexpression_promote hsa-mir-155 Leukemia, Myeloid, Acute 29657293 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 miR-155 overexpression plays a key pathogenic role in some lymphomas and acute myeloid leukemias has led to the development of an antagomir-based approach as a new promising therapeutic strategy genetics_overexpression_promote hsa-mir-181a Leukemia, Myeloid, Acute 27531761 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Overexpression of miR-181a can promote AML cell proliferation. genetics_overexpression_promote hsa-mir-375 Liver Failure 27531059 K72 D017093 613070 HP:0001399 Thus miR-375 is identified as a novel repressor of UGT1A-mediated hepatic acetaminophen glucuronidation through reduced AhR expression, which could predispose some individuals to increased risk for acetaminophen-induced ALF genetics_overexpression_promote hsa-mir-182 Liver Injury 27196584 S36.11 D056486 miR-182, which is associated with disease severity and liver injury. genetics_overexpression_promote hsa-mir-19b Lung Fibrosis 27508324 respiratory system disease DOID:3770 J84.10 D011658 178500 Overexpression of miR-19b in small-airway epithelial cells promoted the mechanical stretch-induced EMT phenotypes, whereas inhibition of miR-19b attenuated it. genetics_overexpression_promote hsa-mir-17 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-18a Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-19a Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-19b-1 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-20a Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-301b Lung Neoplasms 27352910 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 ectopic expression of miR-301b enhanced cell population growth, reduced apoptosis and reduced sensitivity of cells to chemotherapy. genetics_overexpression_promote hsa-mir-92a-1 Lung Neoplasms 17965831 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation. genetics_overexpression_promote hsa-mir-937 Lung Neoplasms 27179609 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Overexpression of miR-937 in A549 promoted anchorage -dependent and -independent growth genetics_overexpression_promote hsa-mir-17 Lymphoma 16940181 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 Mir-17-5p, also known as Mir-91,is located on chromosome 13q31; this gene is amplified in childhoodlymphoma. genetics_overexpression_promote hsa-mir-17 Lymphoma, Burkitt 21981616 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse. genetics_overexpression_promote hsa-mir-18a Lymphoma, Burkitt 21981616 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse. genetics_overexpression_promote hsa-mir-19a Lymphoma, Burkitt 21981616 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse. genetics_overexpression_promote hsa-mir-19b-1 Lymphoma, Burkitt 21981616 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse. genetics_overexpression_promote hsa-mir-20a Lymphoma, Burkitt 21981616 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse. genetics_overexpression_promote hsa-mir-92a-1 Lymphoma, Burkitt 21981616 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse. genetics_overexpression_promote hsa-mir-17 Macular Degeneration 27505139 nervous system disease DOID:4448 H35.30 D008268 PS603075 HP:0000608 Transfection of miR-17-3p mimic in ARPE-19 induced cell death and exacerbated oxidative lethality that was alleviated by miR-17-3p inhibitor. genetics_overexpression_promote hsa-mir-769 Melanoma 27470346 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Overexpression of miR-769 promoted cell proliferation in human melanoma cell line A375, whereas miR-769-in reverses the function. genetics_overexpression_promote hsa-mir-146a Multiple Myeloma 27102001 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 overexpressing miR-146a in MSC, secretion of several cytokines and chemokines including CXCL1, IL6, IL-8, IP-10, MCP-1, and CCL-5 was elevated, resulting in the enhancement of MM cell viability and migration. genetics_overexpression_promote hsa-mir-19a Multiple Myeloma 29665917 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 miR-19a is overexpressed significantly in Lp-1 and U266 multiple myeloma cells, and promots the proliferation and invasion of the myeloma cells, but inhibits their apoptosis genetics_overexpression_promote hsa-mir-125a Myelodysplastic Syndromes 24690917 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 Overexpression of miR-125a in myelodysplastic syndrome CD34+ cells modulates NF-κB activation and enhances erythroid differentiation arrest. genetics_overexpression_promote hsa-mir-196b Myelodysplastic Syndromes 28224273 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 Over-expression of miR-196b-5p is significantly associated with the progression of myelodysplastic syndrome. genetics_overexpression_promote hsa-mir-205 Myelodysplastic Syndromes 27379838 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 Our findings suggest that miR-205-5p upregulation contributes to MDS by suppressing PTEN and that miR-205-5p thus acts as an oncogene in hematopoietic cells. genetics_overexpression_promote hsa-mir-1 Myocardial Infarction 23615185 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Overexpression of MicroRNA-1 improves the efficacy of mesenchymal stem cell transplantation after myocardial infarction. genetics_overexpression_promote hsa-mir-1 Myocardial Infarction 28397788 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Over-expression of microRNA-1 causes arrhythmia by disturbing intracellular trafficking system. genetics_overexpression_promote hsa-mir-34a Myocardial Infarction 22403243 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 IGF-1 significantly inhibited H(2)O(2)-induced miR-34a expression, and miR-34a overexpression abolished the anti-apoptotic effect of IGF-1. genetics_overexpression_promote hsa-mir-195 Myocardial Ischemic-Reperfusion Injury 27019437 D015428 miR-195 expression was upregulated in myocardial I/R injury, and miR-195 overexpression may promote cardiomyocyte apoptosis by targeting Bcl-2 and inducing mitochondrial apoptotic pathway. genetics_overexpression_promote hsa-mir-195 Myocardial Ischemic-Reperfusion Injury 27489501 D015428 Up-regulation of miR-195 in ischemic cardiomyocytes promotes ischemic apoptosis by targeting Bcl-2. genetics_overexpression_promote hsa-mir-30a Nasopharyngeal Neoplasms 24812123 C11.9 D009303 607107 HP:0100630 Furthermore, over-expression of miR-30a transfected with precursor increased the ability of metastasis and invasion of NPC tumor cells in vivo and in vitro. genetics_overexpression_promote hsa-mir-10b Neoplasms [unspecific] 29262659 C80.1 D009369 the overexpression of miR-10b was significantly correlated with metastasis status, and indicated the potential clinical use of miR-10b as a molecular biomarker, particularly in assessing prognosis for patients with cancers genetics_overexpression_promote hsa-mir-15b Neoplasms [unspecific] 27530410 C80.1 D009369 increased miR-15b and decreased RECK expression may contribute to the pathobiology of LYO. genetics_overexpression_promote hsa-mir-17 Neoplasms [unspecific] 20439436 C80.1 D009369 mir-17:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_overexpression_promote hsa-mir-18a Neoplasms [unspecific] 20439436 C80.1 D009369 mir-18a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_overexpression_promote hsa-mir-19a Neoplasms [unspecific] 20439436 C80.1 D009369 mir-19a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_overexpression_promote hsa-mir-19b-1 Neoplasms [unspecific] 20439436 C80.1 D009369 mir-19b:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_overexpression_promote hsa-mir-19b-2 Neoplasms [unspecific] 20439436 C80.1 D009369 mir-19b:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_overexpression_promote hsa-mir-21 Neoplasms [unspecific] 25241894 C80.1 D009369 Ectopic expression of miR-21 and miR-29a promotes angiogenesis and tumor cell proliferation genetics_overexpression_promote hsa-mir-221 Neoplasms [unspecific] 25686829 C80.1 D009369 Over-expression of miR-221 stimulated stem-like cells in luminal type of cancer and the miR-221 level was correlated with clinical outcome in breast cancer patients. genetics_overexpression_promote hsa-mir-374a Neoplasms [unspecific] 25299640 C80.1 D009369 The miR-545/374a cluster encoded in the Ftx lncRNA is overexpressed in HBV-related hepatocellular carcinoma and promotes tumorigenesis and tumor progression. genetics_overexpression_promote hsa-mir-545 Neoplasms [unspecific] 25299640 C80.1 D009369 The miR-545/374a cluster encoded in the Ftx lncRNA is overexpressed in HBV-related hepatocellular carcinoma and promotes tumorigenesis and tumor progression. genetics_overexpression_promote hsa-mir-92a-1 Neoplasms [unspecific] 20439436 C80.1 D009369 mir-92a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_overexpression_promote hsa-mir-92a-2 Neoplasms [unspecific] 20439436 C80.1 D009369 mir-92a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted genetics_overexpression_promote hsa-mir-126 Neovascularization, Pathologic 27203443 D009389 silencing of miR-126-3p repressed angiogenesis, while overexpression of miR-126-5p enhanced angiogenesis. genetics_overexpression_promote hsa-mir-124-1 Neuroblastoma 22123030 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Ectopic overexpression of miR-124 resulted in the downregulation of CDK6, decreased cellular proliferation, and induced cellular morphological changes. genetics_overexpression_promote hsa-mir-124-2 Neuroblastoma 22123030 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Ectopic overexpression of miR-124 resulted in the downregulation of CDK6, decreased cellular proliferation, and induced cellular morphological changes. genetics_overexpression_promote hsa-mir-124-3 Neuroblastoma 22123030 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Ectopic overexpression of miR-124 resulted in the downregulation of CDK6, decreased cellular proliferation, and induced cellular morphological changes. genetics_overexpression_promote hsa-mir-1303 Neuroblastoma 27434867 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 miR-1303 overexpression promoted the proliferation of SH-SY5Y NB cell investigated by MTT assay, colony formation assay and anchorage-independent growth ability assay, while miR-1303 knockdown reduced this effect. genetics_overexpression_promote hsa-mir-21 Neuroblastoma 27285119 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 Forced overexpression of miR-21 significantly increased NB cell proliferation, migration, and invasion. genetics_overexpression_promote hsa-mir-138 Obesity 27762728 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 miR-138/miR-222 Overexpression Characterizes the miRNome of Amniotic Mesenchymal Stem Cells in Obesity. genetics_overexpression_promote hsa-mir-222 Obesity 27762728 disease of metabolism DOID:9970 E66 D009765 601665 HP:0001513 miR-138/miR-222 Overexpression Characterizes the miRNome of Amniotic Mesenchymal Stem Cells in Obesity. genetics_overexpression_promote hsa-mir-196a Oral Neoplasms 25233933 C06.9 D009062 HP:0100649 Functionally, miR-196 actively promoted cell migration and invasion without affecting cell growth. genetics_overexpression_promote hsa-mir-34a Osteoarthritis 27247228 musculoskeletal system disease DOID:8398 M19.9 D010003 165720 HP:0002758 Overexpression of miR-34a promoted apoptosis and inhibited cell proliferation in human chondrocytes genetics_overexpression_promote hsa-mir-196a Osteosarcoma 26045752 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Taken together, miR-196a should be an oncogene in osteosarcoma. The possible mechanism was that overexpression of miR-196a promoted proliferation of MG63 and U2OS cells by modulating the PTEN/PI3K/Akt signaling pathway. genetics_overexpression_promote hsa-mir-21 Osteosarcoma 26779632 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 miR-21 overexpression in MG63 caused a significant raise in cell proliferation and invasion and a significant reduction in cell apoptosis. genetics_overexpression_promote hsa-mir-214 Osteosarcoma 28260089 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Overexpression of miR‑214 promotes the progression of human osteosarcoma by regulating the Wnt/β‑catenin signaling pathway. genetics_overexpression_promote hsa-mir-421 Osteosarcoma 26758431 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 overexpression of miR-421 promoted osteosarcoma cell line MG-63 proliferation, migration, and invasion. genetics_overexpression_promote hsa-mir-488 Osteosarcoma 27376839 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 We also found that exogenous over-expression of microRNA-488 promotes the proliferation, reduces the apoptosis and decreases the sensitivity to chemotherapy (doxorubicin) of osteosarcoma cells genetics_overexpression_promote hsa-mir-664 Osteosarcoma 26515813 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Overexpression of miR-664 was associated with increased migration and invasive abilities of OS cells in vitro genetics_overexpression_promote hsa-mir-9 Osteosarcoma 24969351 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 The findings of our study suggest that increased miR-9 expression has a strong correlation with the aggressive progression of osteosarcoma and its overexpression is a statistically significant risk factor affecting overall survival, suggesting that increased miR-9 expression could be a valuable marker of tumor progression and for prognosis of osteosarcoma. genetics_overexpression_promote hsa-mir-9 Osteosarcoma 27724924 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 MiR-9 is overexpressed in spontaneous canine osteosarcoma and promotes a metastatic phenotype including invasion and migration in osteoblasts and osteosarcoma cell lines. genetics_overexpression_promote hsa-mir-92a Osteosarcoma 28069547 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Overexpression of miR-92a promotes the tumor growth of osteosarcoma by suppressing F-box and WD repeat-containing protein 7. genetics_overexpression_promote hsa-mir-1207 Ovarian Neoplasms 26337084 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 MiR-1207 overexpression promotes cancer stem cell-like traits in ovarian cancer by activating the Wnt/β-catenin signaling pathway. genetics_overexpression_promote hsa-mir-125a Ovarian Neoplasms 19881956 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Overexpression of miR-125a induces conversion of highly invasive ovarian cancer cells genetics_overexpression_promote hsa-mir-130a Ovarian Neoplasms 22455133 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The over expression of miR-130a is associated with cisplatin resistance of ovarian cancer. Inhibiting miR-130a expression may help reverse the cisplatin resistance of ovarian cancer. genetics_overexpression_promote hsa-mir-182 Ovarian Neoplasms 22322863 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 miR-182 overexpression resulted in increased tumor transformation in vitro, and enhanced tumor invasiveness in vitro and metastasis in vivo. The oncogenic properties of miR-182 in ovarian cancer were mediated in part by its impaired repair of DNA double-strand breaks and negative regulation of breast cancer 1 (BRCA1) and metastasis suppressor 1 (MTSS1) expressions as well as its positive regulation of oncogene high-mobility group AT-hook 2 (HMGA2). genetics_overexpression_promote hsa-mir-221 Ovarian Neoplasms 28350128 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Overexpression of miRNA-221 promotes cell proliferation by targeting the apoptotic protease activating factor-1 and indicates a poor prognosis in ovarian cancer. genetics_overexpression_promote hsa-mir-320 Ovarian Neoplasms 28338235 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Overexpression of Hsa-miR-320 Is Associated With Invasion and Metastasis of Ovarian Cancer. genetics_overexpression_promote hsa-mir-429 Ovarian Neoplasms 24802724 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Ectopic over-expression of miR-429 induces mesenchymal-to-epithelial transition (MET) and increased drug sensitivity in metastasizing ovarian cancer cells. genetics_overexpression_promote hsa-mir-433 Ovarian Neoplasms 25684390 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Overexpression of the microRNA miR-433 promotes resistance to paclitaxel through the induction of cellular senescence in ovarian cancer cells. genetics_overexpression_promote hsa-mir-10b Pancreatic Neoplasms 22018284 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 MicroRNA-10b is overexpressed in pancreatic cancer, promotes its invasiveness, and correlates with a poor prognosis. genetics_overexpression_promote hsa-mir-203 Pancreatic Neoplasms 26719072 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 miR-203 promotes proliferation, migration and invasion in pancreatic cancer cells genetics_overexpression_promote hsa-mir-1301 Prostate Neoplasms 27261573 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-1301 promoted cell proliferation of prostate cancer. genetics_overexpression_promote hsa-mir-200a Prostate Neoplasms 22161972 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-200a overexpression reduced prostate cancer cell growth and may have potential, in combination with other markers, in stratifying prostate cancer patients for more intensive monitoring and therapy. genetics_overexpression_promote hsa-mir-221 Prostate Neoplasms 19107213 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-221: The inhibition of the highly expressed miR-221 and miR-222 impairs the growth of prostate carcinoma xenografts in mice genetics_overexpression_promote hsa-mir-222 Prostate Neoplasms 19107213 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-222: The inhibition of the highly expressed miR-221 and miR-222 impairs the growth of prostate carcinoma xenografts in mice genetics_overexpression_promote hsa-mir-296 Prostate Neoplasms 24263102 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Interestingly, ectopic expression of miR-296-3p in P69 increases the tolerance to NK cells whereas knockdown of miR-296-3p in M12 reduces the resistance to NK cells, which both phenotypes can be rescued by re-expression or silencing of ICAM-1 in P69 and M12, respectively. genetics_overexpression_promote hsa-mir-331 Prostate Neoplasms 26259043 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Overexpression of miR-331-3p upregulated mesenchymal markers such as vimentin, N-cadherin, and snail and downregulated epithelial markers such as E-cadherin and desmoplakin in the prostate cancer cell line PC3. genetics_overexpression_promote hsa-mir-9 Pulmonary Hypertension 24615545 cardiovascular system disease DOID:6432 I27.20 D006976 PS178600 HP:0002092 Knockdown of miR-9 followed by hypoxia exposure attenuated PASMCs proliferation and enhanced the expression of contractile genes in vascular smooth muscle cells (VSMCs), while overexpression of miR-9 in normoxia promoted a proliferative phenotype in PASMCs. genetics_overexpression_promote hsa-mir-125b Retinoblastoma 27518550 nervous system disease DOID:768 C69.20 D012175 180200 HP:0009919 overexpression of miR-125b apparently promotes RB cell proliferation and migration in vitro. genetics_overexpression_promote hsa-mir-449a Retinoblastoma 24120948 nervous system disease DOID:768 C69.20 D012175 180200 HP:0009919 We are the first to confirm an inhibitory effect of miR-449a and -449b in retinoblastoma by demonstrating significantly impaired proliferation and increased apoptosis of tumor cells when these miRNAs are overexpressed. genetics_overexpression_promote hsa-mir-125b-1 Rhinosinusitis 22071331 B48.1 Overexpression of miR-125b, a Novel Regulator of Innate Immunity, in Eosinophilic Chronic Rhinosinusitis with Nasal Polyps. genetics_overexpression_promote hsa-mir-125b-2 Rhinosinusitis 22071331 B48.1 Overexpression of miR-125b, a Novel Regulator of Innate Immunity, in Eosinophilic Chronic Rhinosinusitis with Nasal Polyps. genetics_overexpression_promote hsa-mir-34a Sensorineural Hearing Loss 25638533 nervous system disease DOID:10003 H90.5 D006313 304400 In the inner ear HEI-OC1 cell line, miR-34a overexpression inhibited SIRT1, leading to an increase in p53 acetylation and apoptosis. genetics_overexpression_promote hsa-mir-146a Sepsis 23638011 A41.9 D018805 HP:0100806 Overexpression of miR-146a induces a state analogous to tolerance in BLP-stimulated cells and therefore may represent a future target for exogenous modulation of tolerance during microbial infection and sepsis. genetics_overexpression_promote hsa-mir-195 Spinal Cord Injuries 26927342 S34.139A D013119 In addition, Ad-miR-195 also obviously increased the number of apoptotic cells and decreased the neurological recovery in the animals injected with Ad-miR-195. genetics_overexpression_promote hsa-mir-184 Squamous Cell Carcinoma 18451220 disease of cellular proliferation DOID:1749 D002294 Overexpression of miR-184 might play an oncogenic role in the antiapoptotic and proliferative processes of tongue SCC. In addition, plasma miR-184 levels were associated with the presence of primary tumor. genetics_overexpression_promote hsa-mir-1288 Squamous Cell Carcinoma, Esophageal 27658568 disease of cellular proliferation DOID:3748 C562729 Overexpression of miR-1288 play a key role in thepathogenesis of ESCCs and its modulation may have potential therapeutic value in patients with ESCC genetics_overexpression_promote hsa-mir-18a Squamous Cell Carcinoma, Esophageal 27291152 disease of cellular proliferation DOID:3748 C562729 upregulation of miR-18a promoted cell proliferation by increasing cylin D1 genetics_overexpression_promote hsa-mir-223 Squamous Cell Carcinoma, Esophageal 22108521 disease of cellular proliferation DOID:3748 C562729 Overexpression of microRNA-223 regulates the ubiquitin ligase FBXW7 in oesophageal squamous cell carcinoma. genetics_overexpression_promote hsa-mir-373 Squamous Cell Carcinoma, Esophageal 27073718 disease of cellular proliferation DOID:3748 C562729 Overexpression of miR-373 in ECA109 cells enhanced proliferation, G1-phase cell proportion, migration, and invasion. genetics_overexpression_promote hsa-mir-93 Squamous Cell Carcinoma, Esophageal 26273410 disease of cellular proliferation DOID:3748 C562729 The introduction of miR-93 significantly promotes cell proliferation,cell cycle progression, and the metastatic capability of EC109 cells. genetics_overexpression_promote hsa-mir-182 Squamous Cell Carcinoma, Head and Neck 27744260 disease of cellular proliferation DOID:5520 C76.0 C535575 Overexpression of TP53 mutation-associated microRNA-182 promotes tumor cell proliferation and migration in head and neck squamous cell carcinoma. genetics_overexpression_promote hsa-mir-184 Squamous Cell Carcinoma, Head and Neck 25351569 disease of cellular proliferation DOID:5520 C76.0 C535575 Treatment with the precursors of these miRNAs increases the proliferation and migration of HNSCC cells. genetics_overexpression_promote hsa-mir-196a Squamous Cell Carcinoma, Head and Neck 25860510 disease of cellular proliferation DOID:5520 C76.0 C535575 These results show that miR-196a and HOXB9 are overexpressed,perhaps co-ordinately, as HNSCC develops and exert a pro-tumourigenic phenotype in HNSCC and OPM cells. genetics_overexpression_promote hsa-mir-31 Squamous Cell Carcinoma, Head and Neck 27528032 disease of cellular proliferation DOID:5520 C76.0 C535575 miR-31 associated oncogenicities were rescued by ARID1A expression in HNSCC cells. genetics_overexpression_promote hsa-mir-451 Squamous Cell Carcinoma, Head and Neck 26506880 disease of cellular proliferation DOID:5520 C76.0 C535575 And overexpression of miRNA-451 in cells with low endogenous expression of miRNA-451 accelerated proliferation. genetics_overexpression_promote hsa-mir-675 Squamous Cell Carcinoma, Head and Neck 27994496 disease of cellular proliferation DOID:5520 C76.0 C535575 Overexpression of lncRNA H19/miR-675 promotes tumorigenesis in head and neck squamous cell carcinoma. genetics_overexpression_promote hsa-mir-211 Squamous Cell Carcinoma, Oral 27221705 disease of cellular proliferation DOID:0050866 Induction of oral carcinogenesis in transgenic mice using 4-nitroquinoline 1-oxide (4NQO) resulted in more extensive and severe tongue tumorigenesis compared with control animals. genetics_overexpression_promote hsa-let-7a Systemic Lupus Erythematosus 24240124 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 our results suggest that overexpression of let-7a may contribute to hyperplasia and the proinflammatory response in SLE. genetics_overexpression_promote hsa-mir-221 Thyroid Neoplasms 22855362 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Overexpression of miR-221 is associated with aggressive clinicopathologic characteristics and the BRAF mutation in papillary thyroid carcinomas. genetics_overexpression_promote hsa-mir-18a Toxic Epidermal Necrolysis 24184144 disease by infectious agent DOID:9063 L51.2 D013206 608579 Our results indicated that downregulated BCL2L10 caused by miR-18a-5p overexpression mediates intrinsic keratinocyte apoptosis in patients with TEN. Serum miR-18a-5p levels can be a useful disease marker for drug eruptions. genetics_overexpression_promote hsa-mir-18a Urinary Bladder Cancer 21388952 urinary system disease DOID:11054 C67 D001749 109800 Specific deletion of p53 in urothelial cells is associated with specific overexpression of miR-18a and miR-19a and down-regulation of miR-107. genetics_overexpression_promote hsa-mir-19a Urinary Bladder Cancer 21388952 urinary system disease DOID:11054 C67 D001749 109800 Specific deletion of p53 in urothelial cells is associated with specific overexpression of miR-18a and miR-19a and down-regulation of miR-107. genetics_overexpression_promote hsa-mir-15b Uterine Leiomyoma 27530410 D25.9 D007889 150699 HP:0000131 Our findings suggest that miR-15b negatively regulates RECK expression in LYO, and increased miR-15b and decreased RECK expression may contribute to the pathobiology of LYO. genetics_overexpression_promote hsa-mir-20a Uveal Melanoma 27356499 C536494 155720 HP:0007716 miR鈥?0a mimics were transfected into UM cells, which led to increases in cell growth, migration and invasion activities. genetics_overexpression_promote hsa-mir-1908 Wound Healing 27256397 D014945 HP:0001058 miR-1908 had a positive role in scar formation genetics_overexpression_suppress hsa-mir-210 Acute Ischemic Stroke 27390218 cardiovascular system disease DOID:224 I63.9 D002546 HP:0002140 Lentivirus-mediated miR-210 overexpression enhanced the microvessel density and the number of neural progenitor cells in the ischemic mouse brain (P < 0.05) and improved neurobehavioral outcomes in the ischemic mouse (P < 0.05). genetics_overexpression_suppress hsa-mir-16 Acute Lung Injury 22185353 S27 D055371 Accordingly, over-expression of miR-16 could significantly suppress the luciferase activity of reporter fusion with the binding sites of TNFα in its 3'UTR region, suggesting that miR-16 played its role in LPS-induced lung inflammation by a direct manner. genetics_overexpression_suppress hsa-mir-21 Acute Myocardial Infarction 26978580 cardiovascular system disease DOID:9408 I21 D056989 608446 HP:0001658 combination of miR-21 and miR-146a has a greater protective effect against cardiac ischemia/hypoxia-induced apoptosis genetics_overexpression_suppress hsa-mir-449a Adenocarcinoma, Gastric 24260067 disease of cellular proliferation DOID:3717 D37.1 D013274 The overexpression of miR-449a inhibited gastric adenocarcinoma cell growth and promoted cell apoptosis in the MGC-803 and SGC-7901 gastric adenocarcinoma cell lines. genetics_overexpression_suppress hsa-mir-16 Adenocarcinoma, Lung 26064212 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 enforced expression of mir-16 lead to reduced A549 cell proliferation and promote apoptosis. genetics_overexpression_suppress hsa-mir-30a Adenocarcinoma, Lung 26837415 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 overexpression of miR-30a in A549 cells inhibited migration and invasion but not cell proliferation and cell cycle progression genetics_overexpression_suppress hsa-mir-31 Adenocarcinoma, Lung 26299665 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 overexpression of miR-31 led to the inhibition of adenocarcinoma cell proliferation. genetics_overexpression_suppress hsa-mir-519d Adenocarcinoma, Lung 28351305 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 Overexpression of miR-519d in lung adenocarcinoma inhibits cell proliferation and invasion via the association of eIF4H. genetics_overexpression_suppress hsa-mir-95 Adenocarcinoma, Lung 25971210 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 Overexpression of microRNA-95-3p suppresses brain metastasis of lung adenocarcinoma through downregulation of cyclin D1. genetics_overexpression_suppress hsa-mir-192 Adenocarcinoma, Pancreatic Ductal 27216198 disease of cellular proliferation DOID:3498 C25.3 D021441 260350 overexpression of miR-192 was sufficient to reduce cell proliferation and invasion. genetics_overexpression_suppress hsa-mir-193b Adenovirus Infection 25854561 B34.0 D000257 The over-expression of miR-193b may suppress the proliferation of K562 cells. genetics_overexpression_suppress hsa-mir-194 Adenovirus Infection 28618953 B34.0 D000257 Overexpression of microRNA-194 suppresses the epithelial-mesenchymal transition in targeting stem cell transcription factor Sox3 in endometrial carcinoma stem cells. genetics_overexpression_suppress hsa-mir-7 Adrenal Cortex Neoplasms 26452132 disease of cellular proliferation DOID:0050891 C74.0 D000306 HP:0100641 microRNA-7-5p (miR-7) reduces cell proliferation in vitro and induces G1 cell cycle arrest. genetics_overexpression_suppress hsa-mir-126 Age-Related Macular Degeneration 27338342 nervous system disease DOID:10871 H35.30 D008268 PS603075 overexpression effects of miR-126 were also proven on human microvascular endothelial cells genetics_overexpression_suppress hsa-mir-155 Allergy 27497617 immune system disease DOID:1205 T78.40 D006967 HP:0012393 miR-155 overexpression significantly suppressed IL-13-induced secretion of CCL11 and CCL26. genetics_overexpression_suppress hsa-mir-16 Alzheimer Disease 26592823 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 Overexpression and inhibition of miR-16 in the cellular AD model with primary hippocampal neurons decreased and increased apoptosis genetics_overexpression_suppress hsa-mir-34a Alzheimer Disease 26459758 nervous system disease DOID:10652 G30.9 D000544 104300 HP:0002511 Importantly, the overexpression of TAp73伪 and miR-34a reversed cell cycle-related neuronal apoptosis (CRNA). genetics_overexpression_suppress hsa-mir-155 Arthritis 24708712 musculoskeletal system disease DOID:848 M19.90 D001168 Overexpression of miR-155 in the gouty SFMC leads to suppress SHIP-1 levels and enhance proinflammatory cytokines. genetics_overexpression_suppress hsa-mir-23b Asthma 26748386 respiratory system disease DOID:2841 J45 D001249 600807 HP:0002099 Overexpression of miR-23b significantly inhibited TGF-尾1-induced ASMCs proliferation and promoted apoptosis. genetics_overexpression_suppress hsa-mir-221 Astrocytoma 26191177 disease of cellular proliferation DOID:3069 C72.9 D001254 155755 HP:0009592 Overexpression of miR-221 inhibits proliferation and promotes apoptosis of human astrocytoma cells. genetics_overexpression_suppress hsa-mir-106b Atherosclerosis 27270534 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Overexpression of miR-106b-5p with miR-106b-5p mimic inhibited PTEN expression and TNF-伪-induced apoptosis in HUVEC. genetics_overexpression_suppress hsa-mir-126 Atherosclerosis 27180261 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 miR-126 up-regulation activates EPCs and ECs and contributes to vascular healing and neovessel formation genetics_overexpression_suppress hsa-mir-126 Atherosclerosis 27827458 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 MicroRNA-126 overexpression rescues diabetes-induced impairment in efferocytosis of apoptotic cardiomyocytes. genetics_overexpression_suppress hsa-mir-146a Atherosclerosis 21329689 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Over-expression of miR-146a may be useful in the prevention and treatment of atherosclerosis. genetics_overexpression_suppress hsa-mir-146a Atherosclerosis 25904598 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 cellular enrichment of miR-146a through the systemic delivery of miR-146a mimetics in Apoe(-/-)Ldlr(-/-) and Ldlr(-/-) mice attenuated monocyte/macrophage activation and atherosclerosis in the absence of plasma lipid reduction. genetics_overexpression_suppress hsa-mir-150 Atherosclerosis 27216461 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 The suppressive effects of miR-150 on macrophage foam cell formation are mediated through targeting of AdipoR2. genetics_overexpression_suppress hsa-mir-181b Atherosclerosis 24084690 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 overexpression of miR-181b in the aortic intima of apolipoprotein E-deficient mice and suppressed NF-κB signaling revealed by bioluminescence imaging and reduced target gene expression in the aortic arch in apolipoprotein E-deficient/NF-κB-luciferase transgenic mice. genetics_overexpression_suppress hsa-mir-21 Atherosclerosis 24502419 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Further analysis confirmed that overexpression of miR-21 by transfection with miR-21 mimics notably attenuated lipid accumulation and lipid-laden foam cell formation in LPS-stimulated macrophages, which was reversely up-regulated when silencing miR-21 expression via anti-miR-21 inhibitor transfection, indicating a reverse regulator of miR-21 in LPS-induced foam cell formation. genetics_overexpression_suppress hsa-mir-140 Biliary Tract Neoplasms 27155525 disease of cellular proliferation DOID:0050625 C24.9 D001661 HP:0100574 Ectopic expression of miR-140-5p markedly decreased SEPT2 protein concentration in BTC cells and suppressed cell proliferation and colony formation in vitro. genetics_overexpression_suppress hsa-mir-1180 Bladder Neoplasms 27112784 C67 D001749 109800 HP:0009725 miR-1180-5p also suppressed the tumor growth in vivo significantly genetics_overexpression_suppress hsa-mir-122 Bladder Neoplasms 27508026 C67 D001749 109800 HP:0009725 Furthermore, miR-122 over-expression decreases bladder cancer cell migration, invasion, colony formation in vitro and slow bladder cancer growth and angiogenesis in vivo. genetics_overexpression_suppress hsa-mir-125b Bladder Neoplasms 26807182 C67 D001749 109800 HP:0009725 Overexpression of miR-125b inhibited cellular growth, suppressed cellular migration and caused an accumulation of cells in the G1 phase of the cell cycle genetics_overexpression_suppress hsa-mir-139 Bladder Neoplasms 27355528 C67 D001749 109800 HP:0009725 Gain-of-function studies showed that miR-139-5p and miR-139-3p significantly inhibited cell migration and invasion by BC cells. genetics_overexpression_suppress hsa-mir-26b Bladder Neoplasms 27310702 C67 D001749 109800 HP:0009725 Restoration of these miRNAs inhibited cell migration and invasion in BC. genetics_overexpression_suppress hsa-mir-335 Bladder Neoplasms 27356628 C67 D001749 109800 HP:0009725 Overexpression of miR鈥?35 in T24 cells inhibited cell proliferation and induced apoptosis genetics_overexpression_suppress hsa-mir-429 Bladder Neoplasms 27058893 C67 D001749 109800 HP:0009725 Exogenous mimic of miR-429 treatment dramatically inhibited the migratory ability of T24 cells. genetics_overexpression_suppress hsa-mir-99a Bladder Neoplasms 24944696 C67 D001749 109800 HP:0009725 It was found that miRNA-99a inhibits cell proliferation, migration and invasion in T24 and EJ cells. genetics_overexpression_suppress hsa-mir-203 Brain Disease [unspecific] 25723469 nervous system disease DOID:936 G93.40 D001927 608033 enforced expression of miR-203 or MyD88 siRNA silencing inhibits downstream NF-κβ signaling and microglia activation genetics_overexpression_suppress hsa-let-7a Breast Neoplasms 25846193 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Cell proliferation, colony formation, migration and invasion were decreased after overexpression of let-7a in breast cancer cells and vice versa. genetics_overexpression_suppress hsa-mir-107 Breast Neoplasms 24482686 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Overexpression of miR-107 suppressed MDA-MB-231 cell proliferation and migration, meanwhile the cells were arrested at G0/G1 phase. genetics_overexpression_suppress hsa-mir-143 Breast Neoplasms 26618772 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Up-regulating miR-143 enhanced E-cadherin-mediated cell-cell adhesion ability, reduced mesenchymal markers, and decreased cell proliferation, migration, and invasion in vitro. genetics_overexpression_suppress hsa-mir-145 Breast Neoplasms 26715279 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Overexpression of miR-145 in MCF-7 and BT-549 cell lines significantly inhibited cell proliferation, migration, and invasion in vitro. genetics_overexpression_suppress hsa-mir-145 Breast Neoplasms 27508031 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Wound healing assay and transwell migration assay showed that ectopic expression of miR-145 significantly inhibited breast cancer cell migration. genetics_overexpression_suppress hsa-mir-145 Breast Neoplasms 29425746 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-145 overexpression triggers alteration of the whole transcriptome and inhibits breast cancer development genetics_overexpression_suppress hsa-mir-148a Breast Neoplasms 26707142 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 The ectopic miR-148a expression inhibited the migration and invasion of MCF-7 and MDA-MB-231 breast cancer cells. genetics_overexpression_suppress hsa-mir-148b Breast Neoplasms 27328731 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Depleting miR-214 or elevating miR-148b blocked the dissemination of melanoma or breast cancer cells, an effect that could be accentuated by dual alteration. genetics_overexpression_suppress hsa-mir-16 Breast Neoplasms 25672252 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Overexpression of microRNA-16 declines cellular growth, proliferation and induces apoptosis in human breast cancer cells. genetics_overexpression_suppress hsa-mir-195 Breast Neoplasms 26632252 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 ectopic expression of hsa-miR-195 in MCF-7 and MDA-MB-231 cells not only altered cellular cholesterol and triglyceride levels significantly but also resulted in reduced proliferation, invasion and migration. genetics_overexpression_suppress hsa-mir-199a Breast Neoplasms 27094578 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Overexpression of miR-199a-5p reduced the mRNA and protein levels of Ets-1 in MCF-7 and MDA-MB-231 cells, whereas anti-miR-199a-5p elevated Ets-1. genetics_overexpression_suppress hsa-mir-223 Breast Neoplasms 26876200 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 both RT-induced miR-223 and peri-operative inhibition of EGFR efficiently prevented BC cell growth and reduced recurrence formation in mouse models of BC. genetics_overexpression_suppress hsa-mir-302b Breast Neoplasms 26623722 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-302b overexpression enhances sensitivity to cisplatin in breast cancer cell lines, reducing cell viability and proliferation in response to the treatment. genetics_overexpression_suppress hsa-mir-340 Breast Neoplasms 26758430 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-340 could dramatically down-regulate metastasis by targeting Wnt signaling in breast cancer cells. genetics_overexpression_suppress hsa-mir-378 Breast Neoplasms 26749280 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 ectopic expression of miR-378 in MDA-MB-231 cells inhibited Runx1 and suppressed migration and invasion, while inhibition of miR-378 in MCF7 cells increased Runx1 levels and cell migration. genetics_overexpression_suppress hsa-mir-410 Breast Neoplasms 27221455 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-410-3p overexpression reduced cell growth, colony formation and the number of EdU-positive cells in the MDA-MB-231 cells. genetics_overexpression_suppress hsa-mir-411 Breast Neoplasms 27264952 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Ectopic expression of miR-411-5p suppressed the breast cancer cell proliferation genetics_overexpression_suppress hsa-mir-486 Breast Neoplasms 24104550 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 in vitro functional screening of the downregulated miRNAs in non-malignant and breast cancer cell lines identified several possible tumor suppressor miRNAs, including miR-193b, miR-193a-3p, miR-126, miR-134, miR-132, miR-486-5p, miR-886-3p, miR-195 and miR-497, showing reduced growth when re-expressed in cancer cells genetics_overexpression_suppress hsa-mir-497 Breast Neoplasms 27303812 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Enforced miR-497 expression, accompanied with SMAD7 reduction, suppressed MDA-MB-231 and MCF-7 breast cancer cell growth genetics_overexpression_suppress hsa-mir-497 Breast Neoplasms 27456360 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Further, overexpression of miR-497 not only inhibited ERR伪 expression but also reduced MIF level and MMP9 activity, which led to significant decreases in cell proliferation, migration, and invasion of ER伪 negative breast cancer. genetics_overexpression_suppress hsa-mir-502 Breast Neoplasms 27080302 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Treatment with miR-502 or downregulation of SET8 suppressed cell proliferation and cell cycle, and reduced cell migration, invasion and EMT. genetics_overexpression_suppress hsa-mir-506 Breast Neoplasms 26059632 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 MiR-506 over-expression significantly inhibits the proliferation,colony formation, and migration of breast cancer cells. miR-506 over-expression may thus be able to improve the malignant phenotype of breast cancer cells. genetics_overexpression_suppress hsa-mir-613 Breast Neoplasms 27449609 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-613 mimics significantly inhibited the migration and invasion of breast cancer cells, whereas miR-613 inhibitors significantly increased cell migration and invasion. genetics_overexpression_suppress hsa-mir-101 Carcinoma, Bladder 27485165 urinary system disease DOID:4007 D09.0 D001749 109800 HP:0002862 In addition, plasmid鈥憁ediated overexpression of miR鈥?01 and small hairpin RNA鈥憁ediated inhibition of c鈥慒OS significantly inhibited the proliferation and invasive capacity of T24 cells. genetics_overexpression_suppress hsa-mir-106a Carcinoma, Bladder 27513725 urinary system disease DOID:4007 D09.0 D001749 109800 HP:0002862 Overexpression of mir-106a suppressed the proliferation of bladder cancer cell in EJ. genetics_overexpression_suppress hsa-mir-205 Carcinoma, Breast 27468619 D05 D001943 114480 HP:0003002 Knock-up of miR-205 expression by transfection with its mimics promoted MDA-MB-468 cells apoptosis (P=0.006 1). genetics_overexpression_suppress hsa-mir-26a Carcinoma, Breast 27517917 D05 D001943 114480 HP:0003002 MiR-26a overexpression resulted in a reduction in cell viability that was partially recovered by inhibiting it. genetics_overexpression_suppress hsa-mir-34a Carcinoma, Breast 27524218 D05 D001943 114480 HP:0003002 MiR-34a expression was remarkably down-regulated in BC tissues and cell lines compared with normal tissues and cell lines. genetics_overexpression_suppress hsa-mir-365 Carcinoma, Breast 27906431 D05 D001943 114480 HP:0003002 Overexpression of microRNA-365 inhibits breast cancer cell growth and chemo-resistance through GALNT4. genetics_overexpression_suppress hsa-mir-145 Carcinoma, Breast, Triple Negative 26733177 D064726 tumor necrosis factor-alpha (TNF-伪)-induced apoptosis was expanded by the transfection of miR-145 in MDA-MB-231 which belongs to the TNBC cell lines. genetics_overexpression_suppress hsa-mir-145 Carcinoma, Breast, Triple Negative 27364572 D064726 Upregulating miR-145 in HCC1937 cells dramatically suppressed cell proliferation and induced G1-phase arrest genetics_overexpression_suppress hsa-mir-18a Carcinoma, Breast, Triple Negative 27338042 D064726 Enforced miR-18a overexpression directly led to increased autophagy in MDA-MB-231 cells genetics_overexpression_suppress hsa-mir-200 Carcinoma, Breast, Triple Negative 27402080 D064726 miR-9 and miR-200 promoted and inhibited, respectively, the formation of vascular-like structures in vitro genetics_overexpression_suppress hsa-mir-206 Carcinoma, Breast, Triple Negative 27318091 D064726 The miR-206 mimics inhibited TNBC breast cell invasion and angiogenesis. genetics_overexpression_suppress hsa-mir-490 Carcinoma, Breast, Triple Negative 27506313 D064726 Gain-of-function studies revealed that miR-490-3p-3p overexpression inhibited cell growth and invasion in both MDA-MB-231 and MDA-MB-436 TNBC cells and impaired tumorigenesis of MDA-MB-231 cells in nude mice. genetics_overexpression_suppress hsa-mir-544 Carcinoma, Breast, Triple Negative 27186677 D064726 overexpression of miR-544 in triple negative breast cancer cells significantly down-regulated expressions of Bcl6 and Stat3, which in turn severely inhibited cancer cell proliferation, migration and invasion in vitro. genetics_overexpression_suppress hsa-mir-139 Carcinoma, Cervical 27505862 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 Overexpression of miR-139-3p significantly suppressed HeLa cell proliferation, migration and invasion and induced cell apoptosis. genetics_overexpression_suppress hsa-mir-148b Carcinoma, Cervical 27505047 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 miR-148b mimics significantly decreased the cell proliferation ability and invasion ability, and statistically induced apoptosis. genetics_overexpression_suppress hsa-mir-200b Carcinoma, Cervical 26935156 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 miR鈥?00b suppressed the migratory potential of cervical carcinoma cells genetics_overexpression_suppress hsa-mir-34a Carcinoma, Cervical 27456356 disease of cellular proliferation DOID:2893 D06.9 D002583 603956 HP:0030159 While forced expression of miR-34a in CaCx and CRC cells inhibited HMGB1 mRNA and protein levels, proliferation, migration and invasion, inhibition of endogenous miR-34a enhanced these tumourigenic properties. genetics_overexpression_suppress hsa-let-7a Carcinoma, Colon 27498032 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 Further studies demonstrated that over-expressed let-7a could remarkably inhibit HCT-116 and SW620 cell growth and metastasis by directly down-regulating Rhotekin (RTKN). genetics_overexpression_suppress hsa-mir-34a Carcinoma, Colon 28035390 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 overexpression of miR-34a may inhibit the proliferation, invasion and metastasis of HCT116 cells genetics_overexpression_suppress hsa-mir-29c Carcinoma, Embryonal 26484393 disease of cellular proliferation DOID:3308 D018236 HP:0002898 MicroRNA-29c overexpression inhibits proliferation and promotes apoptosis and differentiation in P19 embryonal carcinoma cells. genetics_overexpression_suppress hsa-mir-24 Carcinoma, Endometrial 27279639 reproductive system disease DOID:2871 D07.0 D016889 608089 HP:0012114 Up-regulation of miR-24 inhibited the cell proliferation genetics_overexpression_suppress hsa-mir-372 Carcinoma, Endometrial 26673619 reproductive system disease DOID:2871 D07.0 D016889 608089 HP:0012114 miR-372 overexpression suppressed tumor growth genetics_overexpression_suppress hsa-mir-138 Carcinoma, Gallbladder 25962180 disease of cellular proliferation DOID:4948 C23 D005706 Expression of miR-138 is frequently reduced in gallbladder carcinoma when compared to normal cells. Overexpression of miR-138 inhibited cell proliferation by directly suppressing the expression of Bag-1. These results suggest that miR-138 plays an important role in inhibiting the growth of gallbladder carcinoma. genetics_overexpression_suppress hsa-mir-137 Carcinoma, Gastric 27468717 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Over expression of miR-137 could inhibit the cell migration, proliferation, and promote cell cycle arrest in G0/G1 stage in BGC-823 and SGC-7901 cell lines. genetics_overexpression_suppress hsa-mir-148a Carcinoma, Gastric 27518872 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Ectopic expression of miR-148a inhibited tumor cell proliferation and migration in vitro, and inhibited tumor formation in vivo. genetics_overexpression_suppress hsa-mir-18a Carcinoma, Gastric 26622381 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 The results showed that miR-18a overexpression was able to promote cell apoptosis and inhibit cell invasion. genetics_overexpression_suppress hsa-mir-3178 Carcinoma, Gastric 27493095 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 The condition medium from miR-3178 mimic transfected GES-1 cells could inhibit proliferation and induce apoptosis of inflammation-related gastric cancer cells SGC7901 and MGC803 by decreasing the production of inflammatory cytokines TNF-伪 and IL-6, which were secreted by GES-1 cells. genetics_overexpression_suppress hsa-mir-34a Carcinoma, Gastric 27513895 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Upregulation of miR-34a enhanced the DDP sensitivity of SGC7901/DDP cells to DDP through the inhibition of cell proliferation and induction of cell apoptosis. genetics_overexpression_suppress hsa-mir-370 Carcinoma, Gastric 27499479 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 Upregulation of microRNA-370 promotes cell apoptosis and inhibits proliferation by targeting PTEN in human gastric cancer. genetics_overexpression_suppress hsa-mir-449a Carcinoma, Gastric 25202363 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 The level of MGC-803 cell proliferation was decreased and the apoptosis level was increased by the upregulation of miR-449a expression genetics_overexpression_suppress hsa-let-7g Carcinoma, Hepatocellular 25435961 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 the overexpression of let-7g/i significantly suppressed DNA replication, inhibited cell proliferation and promoted apoptosis of BEL-7402 hepatoma cells. genetics_overexpression_suppress hsa-let-7i Carcinoma, Hepatocellular 25435961 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 the overexpression of let-7g/i significantly suppressed DNA replication, inhibited cell proliferation and promoted apoptosis of BEL-7402 hepatoma cells. genetics_overexpression_suppress hsa-let-7i Carcinoma, Hepatocellular 27126374 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Let-7i was downregulated in HCC tissues, and transfection of HuH-7 with let-7i inhibited malignant cell behaviors and decreased IGF2BPs transcripts. genetics_overexpression_suppress hsa-mir-1207 Carcinoma, Hepatocellular 27461404 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-1207-5p significantly suppressed the cell growth and invasion of HCC cells. genetics_overexpression_suppress hsa-mir-125b-1 Carcinoma, Hepatocellular 18649363 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-125b: overexpression of miR-125b in HCC cell line could obviously suppress the cell growth and phosporylation of Akt genetics_overexpression_suppress hsa-mir-125b-2 Carcinoma, Hepatocellular 18649363 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-125b: overexpression of miR-125b in HCC cell line could obviously suppress the cell growth and phosporylation of Akt genetics_overexpression_suppress hsa-mir-1299 Carcinoma, Hepatocellular 27490780 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-1299 overexpression inhibited cell proliferation and arrested cell cycle in G0/G1 phase analyzed by MTT assay, soft agar assay, BrdU cell proliferation assay and cell cycle assay, while miR-1299 knockdown promoted cell proliferation and accelerated G1/S transition. genetics_overexpression_suppress hsa-mir-132 Carcinoma, Hepatocellular 27467251 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The tumor-suppressive role of miR-132 in HCC has been further confirmed by in vitro experiments. genetics_overexpression_suppress hsa-mir-137 Carcinoma, Hepatocellular 27492460 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-137 via adenoviral vector inhibited the proliferation and anchorage-independent growth of HCC cells, HepG2 and MHCC-97H. genetics_overexpression_suppress hsa-mir-141 Carcinoma, Hepatocellular 27412940 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Over-expression of miR-141 inhibits the proliferation, invasion and migration of hepatocellular carcinoma MHCC-97H cells genetics_overexpression_suppress hsa-mir-142 Carcinoma, Hepatocellular 28081734 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 MicroRNA-142-5p Overexpression Inhibits Cell Growth and Induces Apoptosis by Regulating FOXO in Hepatocellular Carcinoma Cells. genetics_overexpression_suppress hsa-mir-145 Carcinoma, Hepatocellular 26615424 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-145 in HCC cell lines significantly inhibited cell proliferation, migration, and invasion in vitro. genetics_overexpression_suppress hsa-mir-149 Carcinoma, Hepatocellular 27300349 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-149 or inhibition of PARP-2 expression could inhibit tumor growth but was more effective in sensitizing chemotherapy and radiotherapy in xenograft HCC animal models genetics_overexpression_suppress hsa-mir-150 Carcinoma, Hepatocellular 26871477 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-150 overexpression inhibited cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo. genetics_overexpression_suppress hsa-mir-15a Carcinoma, Hepatocellular 26581909 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Ectopic overexpression of miR-15a-5p suppressed cancer proliferation, induced cell cycle arrest in HepG2 or SNU-182 cells in vitro, and inhibited HCC tumor growth in vivo. genetics_overexpression_suppress hsa-mir-16 Carcinoma, Hepatocellular 26499886 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The results of this study suggest that the overexpression of miR-16 inhibits the proliferation, invasion and metastasis of HepG2 HCC cells, and that these effects are associated with the PI3K/Akt signaling pathway. genetics_overexpression_suppress hsa-mir-18a Carcinoma, Hepatocellular 27421245 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 We transfected HepG2.2.15 with miR-18a mimics and CTGF siRNA, finding that upregulated miR-18a and downregulated CTGF suppress the viability and cause cell cycle arrest. genetics_overexpression_suppress hsa-mir-192 Carcinoma, Hepatocellular 26684241 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-192 significantly suppressed metastasis of HCC cells in vitro and in vivo. genetics_overexpression_suppress hsa-mir-199a-1 Carcinoma, Hepatocellular 21847633 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Lentivirus-Mediated Overexpression of MicroRNA-199a Inhibits Cell Proliferation of Human Hepatocellular Carcinoma. genetics_overexpression_suppress hsa-mir-199a-2 Carcinoma, Hepatocellular 21847633 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Lentivirus-Mediated Overexpression of MicroRNA-199a Inhibits Cell Proliferation of Human Hepatocellular Carcinoma. genetics_overexpression_suppress hsa-mir-200b Carcinoma, Hepatocellular 26919246 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Forced expression of microRNA-200b in HCC cells dramatically repressed proliferation, colony formation, cell cycle progression, and invasion. genetics_overexpression_suppress hsa-mir-200b Carcinoma, Hepatocellular 26986232 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Upregulated miR鈥?00b expression in HepG2 cells led to a decrease in DNMT3a expression levels, and an inhibition of cell proliferation. genetics_overexpression_suppress hsa-mir-206 Carcinoma, Hepatocellular 24919811 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 MicroRNA-206 overexpression promotes apoptosis, induces cell cycle arrest and inhibits the migration of human hepatocellular carcinoma HepG2 cells. genetics_overexpression_suppress hsa-mir-20a Carcinoma, Hepatocellular 27313460 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 growth of HepG2 cells in the miR-20a mimics group was significantly inhibited genetics_overexpression_suppress hsa-mir-21 Carcinoma, Hepatocellular 27793160 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of microRNA-21 strengthens stem cell-like characteristics in a hepatocellular carcinoma cell line. genetics_overexpression_suppress hsa-mir-214 Carcinoma, Hepatocellular 26498144 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-214 in HCC cells inhibited proliferation by inducing G1-S checkpoint arrest. genetics_overexpression_suppress hsa-mir-214 Carcinoma, Hepatocellular 26788207 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 enhanced expression of miR-214 or silencing of E2F3 inhibited the proliferation of HCC SMMC-7721 cells. genetics_overexpression_suppress hsa-mir-214 Carcinoma, Hepatocellular 27129291 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-214 significantly attenuated cell proliferation. genetics_overexpression_suppress hsa-mir-218 Carcinoma, Hepatocellular 25374061 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-218 inhibits hepatocellular carcinoma cell growth through RET. genetics_overexpression_suppress hsa-mir-26b Carcinoma, Hepatocellular 26891666 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-26b-5p inhibited HCC cell growth and impaired the tube formation ability of the HCC cells genetics_overexpression_suppress hsa-mir-302b Carcinoma, Hepatocellular 26254095 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-302b suppressed HCC cell invasion and metastasis. genetics_overexpression_suppress hsa-mir-30b Carcinoma, Hepatocellular 27333771 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Gain- and loss-of-function studies revealed that miR-30b could dramatically inhibit in vitro HCC cell migration and invasion. genetics_overexpression_suppress hsa-mir-449a Carcinoma, Hepatocellular 27398144 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Ectopic expression of miR-449a suppressed HCC cell proliferation, colony formation, migration and invasion. genetics_overexpression_suppress hsa-mir-451 Carcinoma, Hepatocellular 27461244 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 In this study, overexpression of miR-451 clearly attenuated the promoting effects of HCC cells on cell proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVECs). genetics_overexpression_suppress hsa-mir-663a Carcinoma, Hepatocellular 27261623 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-663a distinctly inhibited cell proliferation, migration and invasion. genetics_overexpression_suppress hsa-mir-7 Carcinoma, Hepatocellular 27391479 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Overexpression of miR-7 inhibited the HCC cell proliferation and invasion. Overexpression of miR-7 could suppress the direct target gene CCNE1 and PIK3CD expression. genetics_overexpression_suppress hsa-mir-92a-1 Carcinoma, Hepatocellular 22587342 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Oxidative DNA damage correlates with cell immortalization and mir-92 expression in hepatocellular carcinoma. genetics_overexpression_suppress hsa-mir-34c Carcinoma, Hepatocellular, HBV-Related 26722295 The restoration of miR-34c in HepG2.2.15 cells suppressed TGIF2 expression, HBV replication and viral antigen synthesis; inhibited cell proliferation; and induced apoptosis. genetics_overexpression_suppress hsa-mir-30b Carcinoma, Laryngeal 25356506 disease of cellular proliferation DOID:2600 C32.3 D007822 21198 HP:0012118 Overexpression of microRNA-30b improves adenovirus-mediated p53 cancer gene therapy for laryngeal carcinoma. genetics_overexpression_suppress hsa-mir-34a Carcinoma, Laryngeal 27220728 disease of cellular proliferation DOID:2600 C32.3 D007822 21198 HP:0012118 expression of miR-34a inhibited cell proliferation and migration in laryngeal carcinoma cells. genetics_overexpression_suppress hsa-mir-107 Carcinoma, Lung 27498977 disease of cellular proliferation DOID:3905 C34.90 D008175 Function assays showed that overexpression of miR-107 suppressed cell proliferation, migration and invasion in A549 cells in vitro, and inhibited NSCLC tumor growth in vivo. genetics_overexpression_suppress hsa-mir-124 Carcinoma, Lung 27251409 disease of cellular proliferation DOID:3905 C34.90 D008175 overexpression of miR-124 in A549 cells suppressed cell migration and invasion activity genetics_overexpression_suppress hsa-mir-29a Carcinoma, Lung 27488440 disease of cellular proliferation DOID:3905 C34.90 D008175 Restoration of miR-29a suppressed cancer cell aggressiveness and fibroblast migration. genetics_overexpression_suppress hsa-mir-509 Carcinoma, Lung 27498003 disease of cellular proliferation DOID:3905 C34.90 D008175 In addition, over-expression of miR-509-3-5p markedly blocked A549 cell proliferation and sensitized the cells to CIS and ADR treatment. genetics_overexpression_suppress hsa-mir-124 Carcinoma, Lung, Non-Small-Cell 27073840 C34.90 D002289 HP:0030358 Overexpression of miR-124 apparently suppressed the proliferation and invasion of NSCLC cell lines in vitro. genetics_overexpression_suppress hsa-mir-124 Carcinoma, Lung, Non-Small-Cell 27376157 C34.90 D002289 HP:0030358 Overexpression of miR-124 significantly suppresses tumor cell proliferation, colony formation, migration, and induction of apoptosis in H322 and A549 cells. genetics_overexpression_suppress hsa-mir-126 Carcinoma, Lung, Non-Small-Cell 27236384 C34.90 D002289 HP:0030358 Upregulation of miR-126 resulted in the decrease of the proliferation, migration, and invasive abilities of A549 cells genetics_overexpression_suppress hsa-mir-134 Carcinoma, Lung, Non-Small-Cell 27241841 C34.90 D002289 HP:0030358 miR-134 suppressed tumour growth of A549 xenograft in nude mice. genetics_overexpression_suppress hsa-mir-143 Carcinoma, Lung, Non-Small-Cell 29630116 C34.90 D002289 HP:0030358 overexpression of miR-143 downregulated cell proliferation, promoted the apoptosis, and suppressed the phosphorylation of EGFR, AKT and ERK1/2; thus, miR-143 may play a role in treatment of NSCLC to enhance therapeutic efficacy genetics_overexpression_suppress hsa-mir-186 Carcinoma, Lung, Non-Small-Cell 27498924 C34.90 D002289 HP:0030358 Furthermore, overexpression of miR-186 suppressed lung cancer cell proliferation, migration and invasion, and induced cell apoptosis. genetics_overexpression_suppress hsa-mir-187 Carcinoma, Lung, Non-Small-Cell 27495872 C34.90 D002289 HP:0030358 Overexpression of miR-187-5p inhibited the growth and metastasis of NSCLC cells. genetics_overexpression_suppress hsa-mir-191 Carcinoma, Lung, Non-Small-Cell 27178817 C34.90 D002289 HP:0030358 cell proliferation was notably reduced by the miR-1908 mimic transfection genetics_overexpression_suppress hsa-mir-200b Carcinoma, Lung, Non-Small-Cell 27356635 C34.90 D002289 HP:0030358 Overexpression of miR鈥?00b significantly inhibited NSCLC cell migration and invasion. genetics_overexpression_suppress hsa-mir-200c Carcinoma, Lung, Non-Small-Cell 26935975 C34.90 D002289 HP:0030358 Overexpression of miR鈥?00c significantly suppressed cell migration and invasion of A549 NSCLC cells. genetics_overexpression_suppress hsa-mir-204 Carcinoma, Lung, Non-Small-Cell 26935060 C34.90 D002289 HP:0030358 Transient over-expression of miR-204 by transfecting with miR-204 mimics suppressed NSCLC cell proliferation, migration, and induced apoptosis and G1 arrest genetics_overexpression_suppress hsa-mir-206 Carcinoma, Lung, Non-Small-Cell 26309565 C34.90 D002289 HP:0030358 Forced overexpression of miR-206 significantly inhibited cell proliferation, migration and invasion of NSCLC cells. genetics_overexpression_suppress hsa-mir-223 Carcinoma, Lung, Non-Small-Cell 27177336 C34.90 D002289 HP:0030358 The overexpression of miR鈥?23 may partially reverse the acquired resistance to epidermal growth factor receptor-TKIs, thus, providing a potential therapeutic strategy for TKI-resistant NSCLC. genetics_overexpression_suppress hsa-mir-26a Carcinoma, Lung, Non-Small-Cell 26492332 C34.90 D002289 HP:0030358 Overexpression of miR-26a in A549 cells inhibited G1-S transition, increased cell death in response to CDDP treatment, and decreased the colony formation of A549 cells. genetics_overexpression_suppress hsa-mir-27b Carcinoma, Lung, Non-Small-Cell 28081743 C34.90 D002289 HP:0030358 Overexpression of MicroRNA-27b Inhibits Proliferation, Migration, and Invasion via Suppression of MET Expression. genetics_overexpression_suppress hsa-mir-320 Carcinoma, Lung, Non-Small-Cell 27277534 C34.90 D002289 HP:0030358 miR鈥?20 inhibited cell growth, migration and invasion in NSCLC cells. genetics_overexpression_suppress hsa-mir-338 Carcinoma, Lung, Non-Small-Cell 27453416 C34.90 D002289 HP:0030358 Forced expression of miR-338-3p in A549 cells led to the suppression of migration/invasion capacity and inhibition of epithelial markers. genetics_overexpression_suppress hsa-mir-452 Carcinoma, Lung, Non-Small-Cell 26718215 C34.90 D002289 HP:0030358 xpression of miR-452 via adenoviral (Ad) vector inhibits the proliferation, invasion, and migration of NSCLC cells A549 or H460. genetics_overexpression_suppress hsa-mir-541 Carcinoma, Lung, Non-Small-Cell 27448300 C34.90 D002289 HP:0030358 We found that expression of miR-541-3p was decreased obviously in NSCLC tissues and plasma. Down-regulation of miR-541-3p was associated with TNM stage and postoperative survival. genetics_overexpression_suppress hsa-mir-34b Carcinoma, Lung, Non-Small-Cell 22593438 C34.90 D002289 HP:0030358 Overexpression of miR-34b significantly reduced cell survival at lower than 4 Gy radiation doses. genetics_overexpression_suppress hsa-let-7a Carcinoma, Nasopharyngeal 25884389 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 synthetic let-7a mimics suppressed NPC cells migration, invasion and EMT process and knockdown of HMGA2 was consistent with the effects of let-7a in NPC cells. genetics_overexpression_suppress hsa-mir-156a Carcinoma, Nasopharyngeal 27341697 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 synthetic miR156a mimic inhibited the EMT of NPC cells in vitro. genetics_overexpression_suppress hsa-mir-15a Carcinoma, Nasopharyngeal 27458095 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 As a result, miR-15a overexpression significantly reduced cell proliferation (p鈥?鈥?.01 or p鈥?鈥?.001) and induced cell apoptosis (p鈥?鈥?.001), while miR-15a suppression got the opposite result for cell proliferation and apoptosis. genetics_overexpression_suppress hsa-mir-16 Carcinoma, Nasopharyngeal 26383521 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 we identified upregulation of tumor suppressor miR-16a, which inhibited cell cycle progression and sensitized NPC cells to chemotherapy. genetics_overexpression_suppress hsa-mir-16 Carcinoma, Nasopharyngeal 26655091 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Ectopic expression of miR-16 suppressed NPC cell proliferation, migration, and invasion in vitro and inhibited tumor growth and metastatic colonization in the lung in vivo. genetics_overexpression_suppress hsa-mir-183 Carcinoma, Nasopharyngeal 28631568 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 MiR-183 overexpression inhibits tumorigenesis and enhances DDP-induced cytotoxicity by targeting MTA1 in nasopharyngeal carcinoma. genetics_overexpression_suppress hsa-mir-183 Carcinoma, Nasopharyngeal 27431799 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Using transient or stable transfection, we showed that ectopic expression of miR-96 and miR-183 suppressed cell growth and tumor sphere formation in NPC. genetics_overexpression_suppress hsa-mir-24 Carcinoma, Nasopharyngeal 26922862 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 cell proliferation was suppressed and radiosensitivity increased when miR-24 was ectopically expressed in NPC cells. genetics_overexpression_suppress hsa-mir-320b Carcinoma, Nasopharyngeal 27428374 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Further studies showed that overexpression of miR-320b suppressed NPC cell proliferation and enhanced mitochondrial fragmentation and apoptosis both in vitro and in vivo, while silencing of miR-320b promoted tumor growth and suppressed apoptosis. genetics_overexpression_suppress hsa-mir-96 Carcinoma, Nasopharyngeal 27431799 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Using transient or stable transfection, we showed that ectopic expression of miR-96 and miR-183 suppressed cell growth and tumor sphere formation in NPC. genetics_overexpression_suppress hsa-mir-148a Carcinoma, Ovarian 27470550 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Moreover, cell experiments confirmed that miR-148a could inhibit proliferation, migration and invasion of ovarian cancer cells. genetics_overexpression_suppress hsa-mir-17 Carcinoma, Ovarian 27499367 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Forced expression of miR-17 led to markedly diminished adhesion and invasion of ovarian cancer cells in vitro, and notably reduced metastatic nodules inside the peritoneal cavity in in vivo SKOV3 xenografts model. genetics_overexpression_suppress hsa-mir-30a Carcinoma, Ovarian 26675258 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Overexpression of miR-30a decreased Akt and mitogen activated protein kinase signaling pathway activation, cell proliferation, invasion, plasticity, EMT marker levels, and vascular endothelial growth factor release. genetics_overexpression_suppress hsa-mir-494 Carcinoma, Ovarian 26695144 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 overexpression of miR-494 in EOC cells could remarkably inhibit proliferation, colony formation, migration, and invasion and induce cell apoptosis, G0/G1 phase arrest. genetics_overexpression_suppress hsa-mir-497 Carcinoma, Ovarian 27513319 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Overexpression of microRNA-497 suppresses cell proliferation and induces apoptosis through targeting paired box 2 in human ovarian cancer. genetics_overexpression_suppress hsa-mir-210 Carcinoma, Pancreatic 27940128 C25.3 C562463 260350 HP:0002894 microRNA-210 overexpression inhibits tumor growth and potentially reverses gemcitabine resistance in pancreatic cancer. genetics_overexpression_suppress hsa-mir-132 Carcinoma, Prostate 27527117 disease of cellular proliferation DOID:10286 D07.5 D011471 176807 HP:0012125 Notably, overexpression of miR-132/212 could inhibit TGF-β (transforming growth factor-β)-induced EMT in Vcap and Lncap cells at both the mRNA and protein expression levels. genetics_overexpression_suppress hsa-mir-212 Carcinoma, Prostate 27527117 disease of cellular proliferation DOID:10286 D07.5 D011471 176807 HP:0012125 Notably, overexpression of miR-132/212 could inhibit TGF-β (transforming growth factor-β)-induced EMT in Vcap and Lncap cells at both the mRNA and protein expression levels. genetics_overexpression_suppress hsa-let-7d Carcinoma, Renal Cell 25193015 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Functional studies indicated that ectopic expression of let-7d significantly inhibited RCC cell proliferation, migration, and peripheral blood monocyte (PBMC) recruitment in vitro, as well as tumor growth, metastasis, and tumor macrophage infiltration in vivo. genetics_overexpression_suppress hsa-mir-184 Carcinoma, Renal Cell 25667660 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Our studies revealed that miR-184 mimic significantly inhibits cell migration, suppresses cell proliferation and induces renal cancer cell apoptosis in vitro when compared with the negative control (P<0.05). genetics_overexpression_suppress hsa-mir-184 Carcinoma, Renal Cell 27431728 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Overexpression of pre-miR-184 changed the metabolic and proliferation features of ccRCC cells by reducing cell glucose consumption, lactate production and cell proliferation. genetics_overexpression_suppress hsa-mir-196a Carcinoma, Renal Cell 27175581 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 miR鈥?96a suppressed cell proliferation, apoptosis and migration of the 786鈥慜 and ACHN RCC cell lines. genetics_overexpression_suppress hsa-mir-205 Carcinoma, Renal Cell 27498834 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 It was revealed that miR鈥?05 promoted the apoptosis of RCC cells and suppressed their proliferation, metastasis and invasion compared with the negative control. genetics_overexpression_suppress hsa-mir-218 Carcinoma, Renal Cell 27314976 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 cell proliferation was suppressed in miR鈥?18 mimic鈥憈ransfected RCC cells compared with control cells genetics_overexpression_suppress hsa-mir-27a Carcinoma, Renal Cell 27313769 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 upregulated miR-27a attenuated RCC tumor growth in the tumor xenograft animal model genetics_overexpression_suppress hsa-mir-34a Carcinoma, Renal Cell 24765202 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The Cell Counting Kit-8 identified that transient forced expression of miR-34a inhibited cell growth and resulted in cell cycle arrest, which was evaluated by flow cytometry. genetics_overexpression_suppress hsa-mir-451 Carcinoma, Renal Cell 26884830 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 microRNA-451 inhibited proliferation, migration and invasion of renal cell carcinomas cells. genetics_overexpression_suppress hsa-mir-141 Carcinoma, Renal Cell, Clear-Cell 27336447 disease of cellular proliferation DOID:4467 HP:0006770 a tumor suppressive effect of miR-141-3p and miR-145-5p by decreasing migration and invasion of RCC cells could be shown. genetics_overexpression_suppress hsa-mir-145 Carcinoma, Renal Cell, Clear-Cell 27336447 disease of cellular proliferation DOID:4467 HP:0006770 a tumor suppressive effect of miR-141-3p and miR-145-5p by decreasing migration and invasion of RCC cells could be shown. genetics_overexpression_suppress hsa-mir-182 Carcinoma, Renal Cell, Clear-Cell 27468875 disease of cellular proliferation DOID:4467 HP:0006770 Compared to the control group, cell viability, colony-forming ability, and numbers of migrated and invaded cells were significantly decreased by transfection with miR-182 mimic but were markedly increased by miR-182 inhibitor (all P < 0.05). genetics_overexpression_suppress hsa-mir-206 Carcinoma, Renal Cell, Clear-Cell 26718123 disease of cellular proliferation DOID:4467 HP:0006770 upregulation of miR-206 inhibited renal cancer cell proliferation, invasion and migration genetics_overexpression_suppress hsa-let-7 Carcinoma, Salivary Adenoid Cystic 27042128 disease of cellular proliferation DOID:4866 C08.9 D003528 the overexpression of miR-98 in ACC-M cells inhibited cell proliferation, invasion, and migration in vitro. genetics_overexpression_suppress hsa-mir-205 Carcinoma, Skin 26527515 disease of cellular proliferation DOID:3451 D04.9 D018280 HP:0008069 Ectopic expression of miR-205-5p in spindle cancer cells reduces Rap1a, mitigates cell invasiveness, decreases proliferation, and delays tumor onset. genetics_overexpression_suppress hsa-mir-29a Carcinoma, Thyroid, Papillary 26482618 disease of cellular proliferation DOID:3969 C73 C536915 188550 HP:0002895 overexpression of miR-29a markedly suppressed PTC cell proliferation, migration, and invasion and promoted PTC apoptosis and cell cycle arrest at G0/G1 phase. genetics_overexpression_suppress hsa-mir-30a Carcinoma, Urothelial 26775686 disease of cellular proliferation DOID:4006 HP:0030409 Both miR-30a and small interfering RNA Notch1 negatively regulated cell proliferation genetics_overexpression_suppress hsa-mir-1 Cardiomegaly 26638879 I51.7 D006332 HP:0001640 miRNA-1 overexpression prevented cardiomyocyte hypertrophy. genetics_overexpression_suppress hsa-mir-181a Cardiomegaly 27221738 I51.7 D006332 HP:0001640 Over-expression of miR-30c or miR-181a decreased expression of p53, p21, ANP, cardiomyocyte cell size, and apoptosis in HG-treated cardiomyocytes. genetics_overexpression_suppress hsa-mir-1 Cardiomyopathy, Hypertrophic 26699910 cardiovascular system disease DOID:11984 I42.2 D002312 192600 HP:0001639 miR-1 mimic, in parallel to CDK6 siRNA, could inhibit PE-induced hypertrophy of NRVCs, with decreases in cell size genetics_overexpression_suppress hsa-mir-133a Cardiomyopathy, Hypertrophic 26403739 cardiovascular system disease DOID:11984 I42.2 D002312 192600 HP:0001639 miR-133a is an important regulator of phenylephrine-induced cardiomyocyte hypertrophy and negatively regulates this process. genetics_overexpression_suppress hsa-mir-218 Cardiomyopathy, Hypertrophic 27258257 cardiovascular system disease DOID:11984 I42.2 D002312 192600 HP:0001639 Overexpression of miR-218 is sufficient to reduce hypertrophy genetics_overexpression_suppress hsa-mir-200a Cardiomyopathy, Ischemic 27573160 I25.5 Overexpression of miR-200a protects cardiomyocytes against hypoxia-induced apoptosis by modulating the kelch-like ECH-associated protein 1-nuclear factor erythroid 2-related factor 2 signaling axis. genetics_overexpression_suppress hsa-mir-124 Cardiovascular Diseases [unspecific] 28849090 D002318 Overexpressed microRNA-506 and microRNA-124 alleviate H2O2-induced human cardiomyocyte dysfunction by targeting krüppel-like factor 4/5. genetics_overexpression_suppress hsa-mir-138 Cardiovascular Diseases [unspecific] 26129883 D002318 over-expression of miR-138 significantly enhanced the cell growth and significantly attenuated the cell apoptosis in hypoxic conditions. genetics_overexpression_suppress hsa-mir-19b Cardiovascular Diseases [unspecific] 23443808 D002318 Overexpression of miR-19b inhibited activation of the Wnt/β-catenin signaling pathway in P19 cells, which may regulate cardiomyocyte differentiation. genetics_overexpression_suppress hsa-mir-27b Cardiovascular Diseases [unspecific] 26161255 D002318 miR-27b mimic had overall beneficial effects genetics_overexpression_suppress hsa-mir-506 Cardiovascular Diseases [unspecific] 28849090 D002318 Overexpressed microRNA-506 and microRNA-124 alleviate H2O2-induced human cardiomyocyte dysfunction by targeting krüppel-like factor 4/5. genetics_overexpression_suppress hsa-mir-99a Cardiovascular Diseases [unspecific] 26914935 D002318 Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy. genetics_overexpression_suppress hsa-mir-210 Cerebral Ischemia 25783636 cardiovascular system disease DOID:2316 I67.82 D002545 HP:0002637 Rats treated with VNS showed increased miR-210 expression as well as decreased apoptosis and antioxidant stress responses compared with the I/R group genetics_overexpression_suppress hsa-mir-24 Cerebral Ischemia 27349868 cardiovascular system disease DOID:2316 I67.82 D002545 HP:0002637 miR-24 overexpression or silencing of neurocan shows an antihypoxic effect in SH-SY5Y cells. genetics_overexpression_suppress hsa-mir-155 Cerebral Malaria 25189739 disease by infectious agent DOID:14069 B50.0 D016779 AAV8-mediated in vivo overexpression of miR-155 enhances the protective capacity of genetically attenuated malarial parasites. genetics_overexpression_suppress hsa-mir-10b Cervical Neoplasms 27296950 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 overexpression of miR-10b in cervical cancer cells could inhibit the cell proliferation and invasion genetics_overexpression_suppress hsa-mir-146b Cervical Neoplasms 25572123 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 miR鈥?46b鈥?p was able to inhibit the proliferative, invasive and adhesive potential and block the cell cycle progression of Caski human cervical cancer cells genetics_overexpression_suppress hsa-mir-152 Cervical Neoplasms 26515145 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 Overexpression of miR-152 repressed WNT1 and ERBB3 expression and decreased proliferation of HeLa cells. genetics_overexpression_suppress hsa-mir-195 Cervical Neoplasms 26622903 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 The expression of miR-195 mimics in the cervical cancer HeLa cell line significantly decreased the cell proliferation, migration and invasion capacities in vitro. genetics_overexpression_suppress hsa-mir-195 Cervical Neoplasms 26631043 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 overexpression of miR-195 played a suppressor role in the proliferation of HeLa and SiHa cells and promoted cell apoptosis. genetics_overexpression_suppress hsa-mir-320 Cervical Neoplasms 26753959 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 miR-320 induces apoptosis via down-regulation of Mcl-1 and activation of caspase-3 but inhibits cell proliferation, migration, invasion, and tumorigenesis in cervical cancer cells. genetics_overexpression_suppress hsa-mir-328 Cervical Neoplasms 27181358 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 Enforced expression of miR-328 led to a decline in the expression of endogenous TCF7L2 in cervical cancer cells. genetics_overexpression_suppress hsa-mir-376c Cervical Neoplasms 27345009 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 Upregulation of miR-376c impaired cell proliferation, blocked G1/S checkpoint of cell cycle and suppressed cell invasion in vitro. genetics_overexpression_suppress hsa-mir-429 Cervical Neoplasms 27133071 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 miR-429 over-expression and inhibition on cell elongation, migration, stress fiber formation, and invasion. genetics_overexpression_suppress hsa-mir-634 Cervical Neoplasms 26367112 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 miR-634 inhibited cell proliferation, migration and invasiveness in cervical cancer cells and the block of miR-634 enhances the mTOR expression at both the mRNA and protein levels which regulated the expression of mTOR negatively. genetics_overexpression_suppress hsa-mir-744 Cervical Neoplasms 27261616 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 up-regulation of miR-744 and down-regulation of Bcl-2 could stimulate Caspase-3 expression, promoting apoptosis of cervical cancer cells. genetics_overexpression_suppress hsa-mir-122 Cholangiocarcinoma 27472451 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 MiR-122 overexpression reduced cell invasion and migration ability, and inhibited cell apoptosis and p53 expression. Inhibiting miR-122 caused the opposite results. genetics_overexpression_suppress hsa-mir-125b Cholangiocarcinoma 26455324 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 We also found that enforced expression of let-7c, miR-99a or miR-125b could reduce the activity of STAT3 and further suppress CCA tumorigenicity in vivo and inhibit the migration and invasion of CCA cells in vitro. genetics_overexpression_suppress hsa-mir-218 Chronic Obstructive Pulmonary Disease 27409149 respiratory system disease DOID:3083 J44.9 D029424 606963 HP:0006510 Perturbation experiments with a miR-218-5p mimic or inhibitor demonstrated a protective role of miR-218-5p in cigarette smoke-induced inflammation and COPD. genetics_overexpression_suppress hsa-mir-132 Chronic Pain 27349406 G89.29 D059350 HP:0012532 Spinal administration of miR-132-3p antagonists via intrathecal (i.t.) catheters dose dependently reversed mechanical allodyina (p<0.001) and eliminated pain behavior genetics_overexpression_suppress hsa-mir-125a Colon Neoplasms 26297542 D12.6 D003110 HP:0100273 overexpression of miR-125a-5p inhibited cell proliferation and induced cell apoptosis in colon cancer cells. genetics_overexpression_suppress hsa-mir-143 Colon Neoplasms 22362069 D12.6 D003110 HP:0100273 Overexpression of three miRNA (miR200c*, miR143*, and miR424*) significantly abrogated invasive potential. genetics_overexpression_suppress hsa-mir-195 Colon Neoplasms 27347317 D12.6 D003110 HP:0100273 Overexpression of miR-195-5p inhibited cellular growth, suppressed cellular migration and invasion, and led to cell cycle arrest at G1 phase in vitro. genetics_overexpression_suppress hsa-mir-200c Colon Neoplasms 22362069 D12.6 D003110 HP:0100273 Overexpression of three miRNA (miR200c*, miR143*, and miR424*) significantly abrogated invasive potential. genetics_overexpression_suppress hsa-mir-205 Colon Neoplasms 27283988 D12.6 D003110 HP:0100273 miR-205 decreases cell proliferation and decreases migratory and invasive potential of colon cancer cells genetics_overexpression_suppress hsa-mir-424 Colon Neoplasms 22362069 D12.6 D003110 HP:0100273 Overexpression of three miRNA (miR200c*, miR143*, and miR424*) significantly abrogated invasive potential. genetics_overexpression_suppress hsa-mir-1 Colorectal Carcinoma 26980745 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The ectopic expression of these miRs induced growth suppression and autophagic cell death genetics_overexpression_suppress hsa-mir-149 Colorectal Carcinoma 27415661 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Re-expression of miR-149 could enhance the 5-FU sensitivity of 5-FU-resistant CRC cells by increasing 5-FU-inducing apoptosis, while downregulation of miR-149 could decrease the 5-FU sensitivity of parental CRC cells by decreasing 5-FU-inducing apoptosis genetics_overexpression_suppress hsa-mir-152 Colorectal Carcinoma 26820128 disease of cellular proliferation DOID:0080199 C19 D015179 114500 restoring the expression of miR-152 in CRC cells dramatically reduced the cell proliferation and cell migration and invasion and promoted apoptosis genetics_overexpression_suppress hsa-mir-195 Colorectal Carcinoma 26064276 disease of cellular proliferation DOID:0080199 C19 D015179 114500 has-miR-195 can promote cell apoptosis and inhibit the invasion and metastasis by inhibiting the expression of Bcl-2. genetics_overexpression_suppress hsa-mir-199b Colorectal Carcinoma 27145368 disease of cellular proliferation DOID:0080199 C19 D015179 114500 restoration of miR-199b considerably reduced cell invasion and migration in vitro and in vivo genetics_overexpression_suppress hsa-mir-19a Colorectal Carcinoma 29207158 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Overexpression of miR-19a inhibits colorectal cancer angiogenesis by suppressing KRAS expression genetics_overexpression_suppress hsa-mir-210 Colorectal Carcinoma 27293381 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-210 mediated the induction of apoptosis genetics_overexpression_suppress hsa-mir-33b Colorectal Carcinoma 26329295 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-33b inhibited tumor cell growth and induced cell cycle arrest. genetics_overexpression_suppress hsa-mir-34a Colorectal Carcinoma 27456356 disease of cellular proliferation DOID:0080199 C19 D015179 114500 While forced expression of miR-34a in CaCx and CRC cells inhibited HMGB1 mRNA and protein levels, proliferation, migration and invasion, inhibition of endogenous miR-34a enhanced these tumourigenic properties. genetics_overexpression_suppress hsa-mir-375 Colorectal Carcinoma 27222350 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-375 inhibited proliferation, invasion and migration in DLD1 and HCT8 cells. genetics_overexpression_suppress hsa-mir-382 Colorectal Carcinoma 26800338 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Transfection with miR-382 mimics impeded the growth, migration, and invasion of CRC cells. genetics_overexpression_suppress hsa-mir-486 Colorectal Carcinoma 27284245 disease of cellular proliferation DOID:0080199 C19 D015179 114500 overexpression of miR-486-5p inhibited the tumor growth and lymphangiogenesis in nude mice genetics_overexpression_suppress hsa-mir-490 Colorectal Carcinoma 27037061 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miR-490-3p suppresses cancer cell proliferation by inducing apoptosis genetics_overexpression_suppress hsa-mir-874 Colorectal Carcinoma 27221209 disease of cellular proliferation DOID:0080199 C19 D015179 114500 expression of miR-874 was downregulated in CRC tissues and cell lines genetics_overexpression_suppress hsa-let-7a-1 Colorectal Carcinoma 22584434 disease of cellular proliferation DOID:0080199 C19 D015179 114500 High let-7a microRNA levels in KRAS-mutated colorectal carcinomas may rescue anti-EGFR therapy effects in patients with chemotherapy-refractory metastatic disease. genetics_overexpression_suppress hsa-let-7a-2 Colorectal Carcinoma 22584434 disease of cellular proliferation DOID:0080199 C19 D015179 114500 High let-7a microRNA levels in KRAS-mutated colorectal carcinomas may rescue anti-EGFR therapy effects in patients with chemotherapy-refractory metastatic disease. genetics_overexpression_suppress hsa-let-7a-3 Colorectal Carcinoma 22584434 disease of cellular proliferation DOID:0080199 C19 D015179 114500 High let-7a microRNA levels in KRAS-mutated colorectal carcinomas may rescue anti-EGFR therapy effects in patients with chemotherapy-refractory metastatic disease. genetics_overexpression_suppress hsa-mir-10a Congenital Diaphragmatic Hernia 25563880 musculoskeletal system disease DOID:3827 Q79.0 D006548 142340 HP:0000776 Human fetal hypoplastic CDH lungs have a specific miR-200/miR-10a signature. Survival after FETO is associated with increased miR-200 family expression. miR-200b overexpression in CDH lungs results in decreased TGF-β/SMAD signaling. genetics_overexpression_suppress hsa-mir-200 Congenital Diaphragmatic Hernia 25563880 musculoskeletal system disease DOID:3827 Q79.0 D006548 142340 HP:0000776 Human fetal hypoplastic CDH lungs have a specific miR-200/miR-10a signature. Survival after FETO is associated with increased miR-200 family expression. miR-200b overexpression in CDH lungs results in decreased TGF-β/SMAD signaling. genetics_overexpression_suppress hsa-mir-200b Congenital Diaphragmatic Hernia 25563880 musculoskeletal system disease DOID:3827 Q79.0 D006548 142340 HP:0000776 Human fetal hypoplastic CDH lungs have a specific miR-200/miR-10a signature. Survival after FETO is associated with increased miR-200 family expression. miR-200b overexpression in CDH lungs results in decreased TGF-β/SMAD signaling. genetics_overexpression_suppress hsa-mir-138 Coronary Artery Disease 28371277 cardiovascular system disease DOID:3393 I20-I25 D003324 608320 Overexpression of microRNA-138 alleviates human coronary artery endothelial cell injury and inflammatory response by inhibiting the PI3K/Akt/eNOS pathway. genetics_overexpression_suppress hsa-mir-330 Cutaneous Melanoma 27363653 disease of cellular proliferation DOID:8923 C43 C562393 PS155600 HP:0012056 Enforced expression of miR-330-5p inhibits malignant CMM cells proliferation and migration and led to downregulation of the TYR and PDIA3 protein. genetics_overexpression_suppress hsa-mir-15a Diabetes Mellitus 27531575 disease of metabolism DOID:9351 E10-E14 D003920 222100 HP:0000819 miR-15a overexpression led to modulation toward nondiabetic levels, rather than complete inhibition of ASM and VEGF-A providing therapeutic effect without detrimental consequences of ASM and VEGF-A deficiencies genetics_overexpression_suppress hsa-mir-29a Diabetes Mellitus 24578127 disease of metabolism DOID:9351 E10-E14 D003920 222100 HP:0000819 Diabetic miR-29a transgenic mice had better nephrin levels, podocyte viability, and renal function and less glomerular fibrosis and inflammation reaction compared with diabetic wild-type mice. genetics_overexpression_suppress hsa-let-7a Diabetes Mellitus, Type 2 24105413 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Expression of microRNA let-7a and let-7d, which are direct translational repressors of the IL-13 gene, was increased in skeletal muscle from T2DM patients. genetics_overexpression_suppress hsa-mir-26a Diabetes Mellitus, Type 2 26208605 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Mir-26a suppresses autoimmune diabetes in NOD mice in part through promoted regulatory T cells (Tregs) expression. genetics_overexpression_suppress hsa-mir-34c Diabetic Nephropathy 26191142 E10-11.21 D003928 miR-34c was downregulated and that overexpression of miR-34c inhibited HG-induced podocyte apoptosis. genetics_overexpression_suppress hsa-mir-15a Diabetic Retinopathy 27531575 nervous system disease DOID:8947 E10-11.31 D003930 Over-expression of miR-15a downregulated, and inhibition of miR-15a upregulated ASM and VEGF-A expression in retinal cells. genetics_overexpression_suppress hsa-mir-27a Endometrial Neoplasms 26934121 reproductive system disease DOID:1380 C54.1 D016889 608089 Enforced expression of miR-124 suppresses EC cell invasion and proliferation. genetics_overexpression_suppress hsa-let-7 Endometriosis 27320036 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 increased let-7f expression effectively reduced the migration of endometrial cells. genetics_overexpression_suppress hsa-let-7f Endometriosis 27320036 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 increased let-7f expression effectively reduced the migration of endometrial cells. genetics_overexpression_suppress hsa-mir-200b Endometriosis 26854065 reproductive system disease DOID:289 N80.0 D004715 131200 HP:0030127 up-regulation of miR-200b reverts EMT, emerging as a potential therapeutic approach to inhibit endometriotic cell motility and invasiveness. genetics_overexpression_suppress hsa-mir-29a Endomyocardial Fibrosis 27060017 cardiovascular system disease DOID:12932 I42.3 D004719 HP:0006685 over-expression of miRNA-29a suppresses cardiac fibroblasts proliferation. genetics_overexpression_suppress hsa-let-7a-1 Esophageal Neoplasms 22363450 C15.9 D004938 133239 HP:0100751 Curcumin treatment down-regulate the expressions of Notch-1 specific microRNAs miR-21 and miR-34a, and upregulated tumor suppressor let-7a miRNA. genetics_overexpression_suppress hsa-let-7a-2 Esophageal Neoplasms 22363450 C15.9 D004938 133239 HP:0100751 Curcumin treatment down-regulate the expressions of Notch-1 specific microRNAs miR-21 and miR-34a, and upregulated tumor suppressor let-7a miRNA. genetics_overexpression_suppress hsa-let-7a-3 Esophageal Neoplasms 22363450 C15.9 D004938 133239 HP:0100751 Curcumin treatment down-regulate the expressions of Notch-1 specific microRNAs miR-21 and miR-34a, and upregulated tumor suppressor let-7a miRNA. genetics_overexpression_suppress hsa-let-7a Ewing Sarcoma 24383407 musculoskeletal system disease DOID:3369 D012512 612219 HP:0012254 Restored let-7a expression inhibited cell proliferation, migration, as well as invasion; arrested cell cycle progression; and induced cell apoptosis of both cell lines. genetics_overexpression_suppress hsa-mir-203 Fatty Liver, Alcoholic 29670525 K70.0 D005235 over-expression of miR-203 inhibited the liver lipids accumulation and the progression of AFL by targeting Lipin1 genetics_overexpression_suppress hsa-mir-26a Fatty Liver, Non-Alcoholic 27377869 disease of metabolism DOID:0080208 K75.81 D065626 613282 LV-26a-infected mice were protected from glucose dysmetabolism and showed markedly decreased total liver weight genetics_overexpression_suppress hsa-let-7 Gastric Neoplasms 25549793 disease of cellular proliferation DOID:10534 C16 D013274 137215 There were significant negative correlations between serum let-7c and its target gene PGC expression genetics_overexpression_suppress hsa-let-7 Gastric Neoplasms 26745603 disease of cellular proliferation DOID:10534 C16 D013274 137215 overexpression of miR-let-7a markedly suppressed the proliferation, migration, and invasion of GC cells by down-regulating the expression of PKM2. genetics_overexpression_suppress hsa-let-7b Gastric Neoplasms 25510669 disease of cellular proliferation DOID:10534 C16 D013274 137215 Ectopic expression of let-7b suppressed the growth, migration, invasion, and tumorigenicity of GC cells, whereas let-7b knockdown promoted these phenotypes. genetics_overexpression_suppress hsa-mir-133b Gastric Neoplasms 24443799 disease of cellular proliferation DOID:10534 C16 D013274 137215 MiR-133b is frequently decreased in gastric cancer and its overexpression reduces the metastatic potential of gastric cancer cells. genetics_overexpression_suppress hsa-mir-137 Gastric Neoplasms 26840256 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-9 and miR-137 downregulated the CUL4A-LATS1-Hippo signaling pathway and suppressed GC cell proliferation and invasion in vitro. genetics_overexpression_suppress hsa-mir-140 Gastric Neoplasms 27353653 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-140 overexpression inhibited HGC-27 cell viability and colony formation and resulted in G0/G1 arrest. genetics_overexpression_suppress hsa-mir-142 Gastric Neoplasms 23209550 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-142-5p and miR-155 in Gastric Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma Resistant to Helicobacter pylori Eradication genetics_overexpression_suppress hsa-mir-155 Gastric Neoplasms 23209550 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-142-5p and miR-155 in Gastric Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma Resistant to Helicobacter pylori Eradication genetics_overexpression_suppress hsa-mir-15a Gastric Neoplasms 26894855 disease of cellular proliferation DOID:10534 C16 D013274 137215 ectopic expression of miR-15a decreased Bmi-1 in gastric cancer cell lines with reduced proliferation and tumor invasion. genetics_overexpression_suppress hsa-mir-27b Gastric Neoplasms 26780940 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-27b overexpression significantly inhibited H. pylori infection-induced cell proliferation and WNT signaling pathway activation in gastric cancer cells. genetics_overexpression_suppress hsa-mir-30a Gastric Neoplasms 27208176 disease of cellular proliferation DOID:10534 C16 D013274 137215 forced miR-30a over-expression in cancer cells can be a potential way to inhibit tumour development. genetics_overexpression_suppress hsa-mir-34a Gastric Neoplasms 24068565 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-34a over-expression could improve the sensitivity of gastric cancer cells against cisplatin-based chemotherapies, with PI3K/AKT/survivin signaling pathway possibly involved in the mechanism. genetics_overexpression_suppress hsa-mir-372 Gastric Neoplasms 26928593 disease of cellular proliferation DOID:10534 C16 D013274 137215 inhibit proliferations of adenocarcinoma gastric cancer (AGS) cells overexpressing these miRNAs genetics_overexpression_suppress hsa-mir-448 Gastric Neoplasms 26852749 disease of cellular proliferation DOID:10534 C16 D013274 137215 Ectopic expression of miR-448 suppressed GC cell proliferation, colony formation, and invasion. genetics_overexpression_suppress hsa-mir-455 Gastric Neoplasms 27451075 disease of cellular proliferation DOID:10534 C16 D013274 137215 re-expression of miR-455-5p could inhibit human GC cell proliferation and invasion, overexpression of miR-455-5p could also promote GC cell apoptosis. genetics_overexpression_suppress hsa-mir-488 Gastric Neoplasms 26738864 disease of cellular proliferation DOID:10534 C16 D013274 137215 The ectopic expression of miR-488 suppressed the GC cell proliferation, cell cycle, colony information, and migration. genetics_overexpression_suppress hsa-mir-9 Gastric Neoplasms 26840256 disease of cellular proliferation DOID:10534 C16 D013274 137215 Overexpression of miR-9 and miR-137 downregulated the CUL4A-LATS1-Hippo signaling pathway and suppressed GC cell proliferation and invasion in vitro. genetics_overexpression_suppress hsa-mir-93 Glaucoma 27878244 nervous system disease DOID:1686 H40 D005901 137750 MicroRNA‑93 is overexpressed and induces apoptosis in glaucoma trabecular meshwork cells. genetics_overexpression_suppress hsa-mir-128 Glioblastoma 21358821 D005909 HP:0100843 Our analysis predicted a significant association between miR-128 and the protein kinase WEE1, which we subsequently validated experimentally by showing that the over-expression of the naturally under-expressed miR-128 in glioma cells resulted in the inhibition of WEE1 in glioblastoma cells. genetics_overexpression_suppress hsa-mir-137 Glioblastoma 27328425 D005909 HP:0100843 overexpression of miR-137 in GBM cells also inhibited cell proliferation, migration, and invasion. genetics_overexpression_suppress hsa-mir-145 Glioblastoma 26374689 D005909 HP:0100843 CSCs expressed low levels of miR-145, and its introduction decreased self-renewal through reductions in AKT signaling and stem cell marker (SOX2, OCT4, and NANOG) expression genetics_overexpression_suppress hsa-mir-146a Glioblastoma 26916895 D005909 HP:0100843 The upregulation of miR-146a in glioma cells through miR-146a mimic transfection led to reduction of cell viability and to an increase in the percentage of apoptosis. genetics_overexpression_suppress hsa-mir-154 Glioblastoma 27013470 D005909 HP:0100843 overexpression of miR-154 suppressed cell migration and invasion of U87 and U251 cells. genetics_overexpression_suppress hsa-mir-155 Glioblastoma 24705102 D005909 HP:0100843 Over-expression of miR-136 and miR-634 miRNAs negatively affected proliferation, but not migration, while expression of miR-155 reduced migration but did not affect the proliferation of LN229 cells. genetics_overexpression_suppress hsa-mir-16 Glioblastoma 26373393 D005909 HP:0100843 Overexpression of microRNA- 16 in the A172 and U87 GBM cell lines inhibited the activities of co-cultured endothelial cells, including proliferation, migration, extension and tubule formation. genetics_overexpression_suppress hsa-mir-203 Glioblastoma 27467502 D005909 HP:0100843 Conversely reconstitution of miR-203 expression induced apoptosis and inhibited migratory property of glioma cells. genetics_overexpression_suppress hsa-mir-203 Glioblastoma 27484906 D005909 HP:0100843 MicroRNA-203 transfected GBM-SCs had reduced capacity for self-renewal in the cell sphere assay and increased expression of glial and neuronal differentiation markers. genetics_overexpression_suppress hsa-mir-29a Glioblastoma 25625222 D005909 HP:0100843 Exogenous miR-29s substantially inhibited the proliferation, migration and invasion of U87MG cells, and promoted their apoptosis. genetics_overexpression_suppress hsa-mir-29a Glioblastoma 28212562 D005909 HP:0100843 Overexpression of miR-29a reduces the oncogenic properties of glioblastoma stem cells by downregulating Quaking gene isoform 6. genetics_overexpression_suppress hsa-mir-7-1 Glioblastoma 26573275 D005909 HP:0100843 In conclusion, our results clearly demonstrated that overexpression of miR-7-1-3p augmented the anti-tumor activities of LUT and SIL to inhibit autophagy and induce apoptosis for controlling growth of different human glioblastomas in vivo. genetics_overexpression_suppress hsa-let-7b Glioma 27520092 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 upregulation of Let-7b, a member of the Let-7 microRNA family, inhibited proliferation, migration, and invasion in glioma cell lines. genetics_overexpression_suppress hsa-let-7f Glioma 25735962 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 The enhanced expression of Let-7f suppressed glioma cells proliferation, migration, and invasion via direct targeting perisotin oncogenic activity. genetics_overexpression_suppress hsa-let-7f Glioma 26750768 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 inhibiting the pro-migratory function of POSTN by the overexpression of miR-Let-7f significantly reduced the formation of VM. genetics_overexpression_suppress hsa-mir-133a Glioma 27154818 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Transfection of miR-150-5p or miR-133a mimics into glioma cell lines reduced MT1-MMP expression and MMP-2 activation by these cells, and cell proliferation and invasion/migration were also suppressed by it. genetics_overexpression_suppress hsa-mir-134 Glioma 27012554 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 upregulated miR-134 expression restrained the proliferation and invasion of U251 cells in vitro. genetics_overexpression_suppress hsa-mir-140 Glioma 27498787 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Restoration of miR-140 obviously suppressed glioma cell proliferation, migration and invasion. genetics_overexpression_suppress hsa-mir-150 Glioma 27154818 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Transfection of miR-150-5p or miR-133a mimics into glioma cell lines reduced MT1-MMP expression and MMP-2 activation by these cells, and cell proliferation and invasion/migration were also suppressed by it. genetics_overexpression_suppress hsa-mir-153 Glioma 27295037 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Exogenous overexpression of miR-153 downregulated Rictor (mRNA and protein) and decreased p-Akt Ser473 in U87MG cells, leading to significant growth inhibition and apoptosis activation. genetics_overexpression_suppress hsa-mir-15b Glioma 27082313 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Furthermore, miR鈥?5b inhibited proliferation and invasion, and promoted apoptosis of glioma cells while downregulating the expression of MMP鈥? and MMP鈥?. genetics_overexpression_suppress hsa-mir-16 Glioma 25511497 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 miR-16 can significantly inhibit the in vivo growth of U87MG glioma. genetics_overexpression_suppress hsa-mir-182 Glioma 26622652 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 overexpression of miR-182 affected cell cycle regulation and cell migration capacity in vitro, which may have been associated with the promotion of apoptosis by this molecule. genetics_overexpression_suppress hsa-mir-34a Glioma 24944883 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Ectopic expression of miR-34a in glioma stem cell-lines HNGC-2 and NSG-K16 decreased the proliferative and migratory potential of these cells, induced cell cycle arrest and caused apoptosis. genetics_overexpression_suppress hsa-mir-34a Glioma 27176117 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Overexpression of miR鈥?4a inhibited proliferation, and induced apoptosis of U87 cells. genetics_overexpression_suppress hsa-mir-370 Glioma 27138069 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Overexpression of miR-370-3p showed a significant inhibitory effect on cell proliferation and accompanied cell cycle G0/G1 arrest in U251 and U87-MG cells. genetics_overexpression_suppress hsa-mir-373 Glioma 26858153 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 although miR-373 does not affect cell growth of U251, it inhibits migration and invasion of U251. genetics_overexpression_suppress hsa-mir-451 Glioma 27476171 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 By targeting CAB 39, miRNA-451 likely triggers the LKB1/AMPK/PI3K/AKT pathway, which regulates GLUT1, to inhibit the glucose metabolism of, reduce the energy supply to, and inhibit the proliferation and invasion of glioma cells. genetics_overexpression_suppress hsa-mir-495 Glioma 27220777 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 restoration of hsa-miR-495 inhibited glioma cell proliferation and invasion in vitro. genetics_overexpression_suppress hsa-mir-508 Glioma 27003587 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 over-expression of miR-508-5p was found to decrease glioma cell growth. genetics_overexpression_suppress hsa-mir-610 Glioma 27485527 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Furthermore, the present study revealed that miR鈥?10 inhibited cell growth, migration and invasion in glioma cells. genetics_overexpression_suppress hsa-mir-26a Graft-Versus-Host Disease 25865461 D89.813 D006086 614395 The prolonged allograft survival induced by LV-Mir-26a was also completely abrogated by IL-6 overexpression. genetics_overexpression_suppress hsa-mir-29b Granular Corneal Dystrophy 27490049 nervous system disease DOID:12318 H18.53 D003317 121900 HP:0007802 Overexpression of miR-29b decreased ECM protein production in human corneal endothelial cells. genetics_overexpression_suppress hsa-mir-363 Head And Neck Neoplasms 26545583 disease of cellular proliferation DOID:11934 C76.0 D006258 HP:0012288 These findings demonstrate that the overexpression of miR-363 reduces cellular migration in head and neck cancer and reveal the biological relationship between miR-363, myosin 1b, and HPV-positive SCCHN. genetics_overexpression_suppress hsa-mir-1 Heart Diseases [unspecific] 27531746 I51.9 D006333 We also found that microRNAs (miRNAs) 1 and 21 bind PLN strongly and relieve PLN inhibition of SERCA to a greater extent than a similar length random sequence RNA mixture. genetics_overexpression_suppress hsa-mir-133a Heart Diseases [unspecific] 27411382 I51.9 D006333 Our results revealed that miR-133a mimic treatment improved the contractility of the diabetic rat's heart concomitant with upregulation of TH, cardiac NE, 尾-AR, and downregulation of TAT and plasma levels of NE. genetics_overexpression_suppress hsa-mir-21 Heart Diseases [unspecific] 27531746 I51.9 D006333 We also found that microRNAs (miRNAs) 1 and 21 bind PLN strongly and relieve PLN inhibition of SERCA to a greater extent than a similar length random sequence RNA mixture. genetics_overexpression_suppress hsa-mir-1 Heart Failure 28063219 I50 D006331 HP:0001635 MicroRNA-1 overexpression blunts cardiomyocyte hypertrophy elicited by thyroid hormone. genetics_overexpression_suppress hsa-mir-132 Heart Failure 29682535 I50 D006331 HP:0001635 Overexpression of microRNA-132 dramatically increased the antioxidant stress and antiapoptotic ability of H9C2 cells and decreased the expression of TGF-β1 and smad3 genetics_overexpression_suppress hsa-mir-133a Heart Failure 25658461 I50 D006331 HP:0001635 transfecting MSCs with miR-133a mimic improves survival of MSCs as determined by the MTT assay. genetics_overexpression_suppress hsa-mir-133a Heart Failure 25960234 I50 D006331 HP:0001635 The miR-133a mimic and miR-133a overexpression significantly caused a decrease in the fibrosis of heart in chronic heart failure rats. genetics_overexpression_suppress hsa-mir-24 Heart Failure 24454859 I50 D006331 HP:0001635 In vivo delivery of miR-24 into a mouse MI model suppressed cardiac cell death, attenuated infarct size, and rescued cardiac dysfunction. genetics_overexpression_suppress hsa-mir-499 Heart Failure 24646523 I50 D006331 HP:0001635 We report that cardiac-abundant miR-499 could protect neonatal rat cardiomyocytes against H 2O 2-induced apoptosis. Increased miR-499 level favored survival, while decreased miR-499 level favored apoptosis. genetics_overexpression_suppress hsa-mir-30a Hepatitis B Virus Infection 25620738 disease by infectious agent DOID:2043 B16/18 D006509 610424 HBx induces autophagosome formation via beclin-1 expression, whereas miRNA-30a overexpression could successfully inhibit the beclin-1 expression induced by HBx, thereby modulating autophagosome formation in hepatic cells. genetics_overexpression_suppress hsa-mir-133a Hypertension 23460283 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 In vitro overexpression of miR-27a,-29a, and -133a inhibited cardiomyocyte hypertrophy and reduced collagen expression. genetics_overexpression_suppress hsa-mir-27a Hypertension 23460283 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 In vitro overexpression of miR-27a,-29a, and -133a inhibited cardiomyocyte hypertrophy and reduced collagen expression. genetics_overexpression_suppress hsa-mir-29a Hypertension 23460283 cardiovascular system disease DOID:10763 I10 D006973 145500 HP:0000822 In vitro overexpression of miR-27a,-29a, and -133a inhibited cardiomyocyte hypertrophy and reduced collagen expression. genetics_overexpression_suppress hsa-mir-200b Hypertrophic Scar 25228082 L91.0 D017439 Overexpression of miR-200b inhibits the cell proliferation and promotes apoptosis of human hypertrophic scar fibroblasts in vitro. genetics_overexpression_suppress hsa-let-7a-1 Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7a-2 Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7a-3 Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7b Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7c Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7d Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7e Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7f-1 Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7f-2 Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7g Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-let-7i Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-mir-98 Hypertrophy 21183740 D006984 Thioredoxin 1 Negatively Regulates Angiotensin II-Induced Cardiac Hypertrophy Through Upregulation of miR-98/let-7. genetics_overexpression_suppress hsa-mir-19a Hypoxia 27220268 D000860 miR-19a overexpression clearly ameliorated hypoxia-induced cell death (necrosis and apoptosis) genetics_overexpression_suppress hsa-mir-210 Hypoxia 26780211 D000860 miR-210 upregulation exerted amelioration on the hypoxia-induced apoptosis genetics_overexpression_suppress hsa-mir-185 Idiopathic Pulmonary Fibrosis 27392970 respiratory system disease DOID:0050156 J84.112 D054990 178500 Furthermore, mimics of miR-185 and miR-186 blocked transforming growth factor-尾-induced collagen V overexpression and alleviated transforming growth factor-尾-induced epithelial-mesenchymal transition in A549 cells and HCC827 cells. genetics_overexpression_suppress hsa-mir-186 Idiopathic Pulmonary Fibrosis 27392970 respiratory system disease DOID:0050156 J84.112 D054990 178500 Our findings suggest that attenuated expression of miR-185 and miR-186 may be responsible for collagen V overexpression during idiopathic pulmonary fibrosis, and these miRNAs may serve as pathogenesis-related biomarkers and treatment targets. genetics_overexpression_suppress hsa-mir-29a Idiopathic Pulmonary Fibrosis 27488440 respiratory system disease DOID:0050156 J84.112 D054990 178500 Restoration of miR-29a suppressed cancer cell aggressiveness and fibroblast migration. genetics_overexpression_suppress hsa-mir-21 Immune System Disease [unspecific] 25688245 immune system disease DOID:2914 D89.9 D007154 miR-21 has emerged as a key mediator of the anti-inflammatory response in macrophages. genetics_overexpression_suppress hsa-mir-223 Inflammation 27148749 D007249 The overexpression of miR-223 in both J774A.1 and peritoneal macrophages induced a phenotypic change from M1 to M2 state genetics_overexpression_suppress hsa-mir-9 Inflammation 26354749 D007249 miR-9 overexpression significantly repressed NF-魏B expression and, thereby, suppressed inflammation but promoted LEC tube formation genetics_overexpression_suppress hsa-mir-210 Intervertebral Disc Degeneration 27284319 musculoskeletal system disease DOID:90 M51 D055959 603932 HP:0008419 downregulation of miR-210 may promote Fas-mediated apoptosis in human IDD by regulating the expression of HOXA9. genetics_overexpression_suppress hsa-mir-497 Invasive Bladder Transitional Cell Carcinoma 27430325 disease of cellular proliferation DOID:6477 C67.9 HP:0006740 We also found that overexpression of miR-497 inhibited the proliferation, migration and invasion of bladder cancer cells by downregulating E2F3 (an miR-497 target gene) mRNA and protein and that siRNA against E2F3 inhibited cell proliferation, migration and invasion, which was similar to the effect of miR-497 overexpression in the BTCC cells. genetics_overexpression_suppress hsa-mir-21 Ischemia 26841045 cardiovascular system disease DOID:326 D007511 601367 over-expressing miR-21 in UCBMSCs could improve neovascularization in CLI genetics_overexpression_suppress hsa-mir-146a Ischemia-Reperfusion Injury 24987958 D015427 Overexpression of miR-146a directly decreased IRAK1 and TRAF6 expression and attenuated the release of proinflammatory cytokines through the inactivation of NF-魏B P65 in hypoxia/reoxygenation (H/R)-induced macrophages, RAW264.7 cells. genetics_overexpression_suppress hsa-mir-150 Ischemia-Reperfusion Injury 29328381 D015427 Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94 genetics_overexpression_suppress hsa-mir-204 Ischemia-Reperfusion Injury 29421577 D015427 overexpression of miR-204 has a protective effect against myocardial I/R injury genetics_overexpression_suppress hsa-mir-21 Ischemia-Reperfusion Injury 25322693 D015427 miR-21 is endowed with anti-apoptotic properties by suppressing the expression of PDCD4 gene and active caspase 3/8 fragments in the condition of renal IRI. genetics_overexpression_suppress hsa-mir-21 Ischemia-Reperfusion Injury 27593550 D015427 Overexpression of microRNA-21 protects spinal cords against transient ischemia. genetics_overexpression_suppress hsa-mir-214 Ischemia-Reperfusion Injury 25593579 D015427 Transfection of miR-214 mimic showed protective effects on OGD-induced injury to H9c2 cells by reducing apoptosis genetics_overexpression_suppress hsa-mir-214 Ischemia-Reperfusion Injury 26025394 D015427 214 may participate in the protective function of ischemic post conditioning by down regulating HIF1AN. genetics_overexpression_suppress hsa-mir-214 Ischemia-Reperfusion Injury 27288437 D015427 Overexpression of the two miRs in cardiomyocytes mimics the effects of carvedilol genetics_overexpression_suppress hsa-mir-221 Ischemia-Reperfusion Injury 26396139 D015427 Mimics of miRNA-221, -150, and -206 were protective in both H9c2 and NRVM. genetics_overexpression_suppress hsa-mir-223 Ischemia-Reperfusion Injury 27502281 D015427 Precursor miR-223 (pre-miR-223) transgenic mouse hearts exhibited better recovery of contractile performance over reperfusion period and lesser degree of myocardial necrosis than wild type hearts upon ex vivo and in vivo myocardial ischemia. genetics_overexpression_suppress hsa-mir-26a Ischemia-Reperfusion Injury 26320674 D015427 Mir-26a overexpression results in attenuated cardiac IR injury and inhibited HMGB1 expression. genetics_overexpression_suppress hsa-mir-497 Ischemia-Reperfusion Injury 27261611 D015427 miR-497 could inhibit inflammation and apoptosis of spinal cord IR through its targets genetics_overexpression_suppress hsa-mir-613 Ischemia-Reperfusion Injury 27534371 D015427 miR-613 inhibits I/R-induced cardiomyocyte apoptosis by targeting PDCD10 by regulating the PI3K/AKT signaling pathway genetics_overexpression_suppress hsa-mir-182 Ischemic Diseases [unspecific] 27008992 D007511 601367 Both exogenous miR-182 and Kenpaullone significantly suppressed hypoxia-induced cardiomyocyte death in vitro. genetics_overexpression_suppress hsa-mir-210 Ischemic Diseases [unspecific] 27530798 D007511 601367 Neonatal rats show down-regulated expression of miRNA-210 after HI, suggesting that miRNA-210 may be involved in the development and progression of hypoxic-ischemic brain edema in neonatal rats. genetics_overexpression_suppress hsa-let-7c Kidney Injury 27203438 S37.0 D058186 miR-let7c-MSC therapy attenuated kidney injury genetics_overexpression_suppress hsa-mir-214 Kidney Neoplasms 27226530 disease of cellular proliferation DOID:263 C64 D007680 miR-214 significantly blocked IGF-1R-forced renal cancer cell proliferation genetics_overexpression_suppress hsa-mir-24 Lacrimal Adenoid Cystic Carcinoma 27351203 nervous system disease DOID:4870 C69.51 overexpression of miR-24-3p decreased its malignant phenotype. genetics_overexpression_suppress hsa-mir-138 Laryngeal Neoplasms 26499780 C32.3 D007822 miR-138 overexpression inhibited ZEB2-mediated cell invasiveness, while miR-138 depletion increased ZEB2-mediated cell invasiveness in LC cells. genetics_overexpression_suppress hsa-mir-143 Leukemia 24626955 C95 D007938 613065 HP:0001909 Overexpression of microRNA-143 inhibits growth and induces apoptosis in human leukemia cells. genetics_overexpression_suppress hsa-mir-143 Leukemia 27492780 C95 D007938 613065 HP:0001909 miRNA143 transfection inhibited K562 cell growth and induced its apoptosis. genetics_overexpression_suppress hsa-mir-181a Leukemia 27517749 C95 D007938 613065 HP:0001909 NP-mediated upregulation of miR-181a led to reduced proliferation, impaired colony formation and increased sensitivity to chemotherapy. genetics_overexpression_suppress hsa-mir-34a Leukemia 27424989 C95 D007938 613065 HP:0001909 Induced expression of miR-34a in TIM3 positive leukemia stem cells (LSC), inhibits the clonogenic expansion, tumor progression and metastasis of leukemia. genetics_overexpression_suppress hsa-mir-663 Leukemia 21518471 C95 D007938 613065 HP:0001909 miRNA-663 in K562 cells is up-regulated after 5-aza treatment. Over-expression of miR-663 can suppress the proliferation of K562 cells, which suggests that miR-663 may possesses suppressive effect for leukaemia. genetics_overexpression_suppress hsa-mir-150 Leukemia, Lymphoblastic, Acute 25687053 disease of cellular proliferation DOID:9952 C91.0 D054198 247640 HP:0006721 miR-150 may be a putative oncoprotein in T-ALL cells. Overexpression of miR-150 has noticeable effects on the proliferation inhibition and apoptosis induction of Jurkat cells, which may be mediated by the negative regulation of PI3K/Akt /NF-κB signaling pathway. genetics_overexpression_suppress hsa-mir-10a Leukemia, Myeloid, Acute 22348345 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 miR-10a is aberrantly overexpressed in Nucleophosmin1 mutated Acute Myeloid Leukaemia and its suppression induces cell death. genetics_overexpression_suppress hsa-mir-125b Leukemia, Myeloid, Acute 28478034 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Overexpression of microRNA-125b inhibits human acute myeloid leukemia cells invasion, proliferation and promotes cells apoptosis by targeting NF-κB signaling pathway. genetics_overexpression_suppress hsa-mir-34b Leukemia, Myeloid, Acute 27296951 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 the miR-34b mimicked transfection-mediated restoration of miR-34b inhibited cell viability and promoted cell apoptosis of HL-60 and OCI-AML3 cell lines. genetics_overexpression_suppress hsa-mir-101 Leukemia, Myeloid, Chronic 27517565 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 These findings suggest that miR-101 acts as a tumor suppressor by downregulating Jak2 expression and sensitizing K562 cells to imatinib. genetics_overexpression_suppress hsa-mir-130a Leukemia, Myeloid, Chronic 27158382 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 over-expression of miR-130a in A562 CML cells dramatically suppresses cell proliferation and induces cell apoptosis both in vitro and in vivo. genetics_overexpression_suppress hsa-let-7b Leukemia-Lymphoma, Precursor T-Cell Lymphoblastic 22918121 disease of cellular proliferation DOID:5599 C83.5 D054218 The enforced expression of let-7b in ALL cell lines with an MLL fusion gene inhibited their growth. genetics_overexpression_suppress hsa-mir-146a Liver Cirrhosis 27399683 endocrine system disease DOID:5082 K74 D008103 215600 HP:0001394 Overexpression of miR-146a-5p inhibited LPS induced pro-inflammatory cytokines secretion through down-regulating the expression levels of TLR-4, IL-1 receptor-associated kinase 1 (IRAK1), TNF receptor associated factor-6 (TRAF6) and phosphorylation of nuclear factor-kappa B (NF-魏B). genetics_overexpression_suppress hsa-mir-29b Liver Cirrhosis 27273381 endocrine system disease DOID:5082 K74 D008103 215600 HP:0001394 miR-29b overexpression inhibited proliferation of LX-2 cells 24鈥塰 after transfection. genetics_overexpression_suppress hsa-mir-20a Liver Diseases [unspecific] 27019188 K76.9 D008107 miR-20a-5p mimic could reverse high glucose-induced impaired glycogenesis and AKT/GSK activation in NCTC1469 and Hep1-6 cells. genetics_overexpression_suppress hsa-mir-145 Liver Fibrosis 27289031 K74 D008103 over-expression of miR-145 inhibited TGF-尾1-induced the activation and proliferation of HSC-T6 cells in vitro. genetics_overexpression_suppress hsa-mir-674 Liver Injury 27313091 S36.11 D056486 miR-674-5p might be a negative regulator in 5-LO mediated autoimmune liver injury genetics_overexpression_suppress hsa-mir-122 Liver Neoplasms 25762642 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 miR-107, mir-122, miR-29, miR-365 and miR-802 exhibited weak to moderate tumor suppressor potential. genetics_overexpression_suppress hsa-mir-15b Liver Neoplasms 26884837 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 MiR-15b mimic transfection promoted miR-15b overexpression and inhibited HepG2 cell proliferation significantly genetics_overexpression_suppress hsa-mir-194 Liver Neoplasms 20979124 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 The overexpression of miR-194 in liver mesenchymal-like cancer cells reduced the expression of the mesenchymal cell marker N-cadherin and suppressed invasion and migration of the mesenchymal-like cancer cells both in vitro and in vivo genetics_overexpression_suppress hsa-mir-449a Liver Neoplasms 26375440 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 Overexpression of miR-449a inhibited cell proliferation, induced G1 phase arrest and cell apoptosis in liver cancer. genetics_overexpression_suppress hsa-mir-7 Liver Neoplasms 24491049 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 Over-expression of miR-7 could significantly inhibit the growth of human lung cancer cells in vivo and in vitro, which might be related to the down-regulated expression of tumor growth-associated protein CGGBP1. genetics_overexpression_suppress hsa-mir-19a Lung Fibrosis 26873752 respiratory system disease DOID:3770 J84.10 D011658 178500 intratracheal application of miR-19a, -19b, and 26b reduced the pulmonary fibrotic severity induced by bleomycin genetics_overexpression_suppress hsa-mir-19b Lung Fibrosis 26873752 respiratory system disease DOID:3770 J84.10 D011658 178500 intratracheal application of miR-19a, -19b, and 26b reduced the pulmonary fibrotic severity induced by bleomycin genetics_overexpression_suppress hsa-mir-221 Lung Fibrosis 27513632 respiratory system disease DOID:3770 J84.10 D011658 178500 miR鈥?21 targets HMGA2 to inhibit bleomycin鈥慽nduced pulmonary fibrosis by regulating TGF鈥懳?/Smad3-induced EMT. genetics_overexpression_suppress hsa-mir-26b Lung Fibrosis 26873752 respiratory system disease DOID:3770 J84.10 D011658 178500 intratracheal application of miR-19a, -19b, and 26b reduced the pulmonary fibrotic severity induced by bleomycin genetics_overexpression_suppress hsa-mir-449a Lung Fibrosis 27351886 respiratory system disease DOID:3770 J84.10 D011658 178500 miR-449a significantly reduced both the distribution and severity of lung lesions induced by silica. genetics_overexpression_suppress hsa-mir-142 Lung Neoplasms 19228723 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-142-5p: were repressed, overexpression can inhibitu lung cancer growth genetics_overexpression_suppress hsa-mir-145 Lung Neoplasms 19228723 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-145: were repressed, overexpression can inhibitu lung cancer growth genetics_overexpression_suppress hsa-mir-146b Lung Neoplasms 21789255 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Overexpression of the Lung Cancer-Prognostic miR-146b MicroRNAs Has a Minimal and Negative Effect on the Malignant Phenotype of A549 Lung Cancer Cells. genetics_overexpression_suppress hsa-mir-196b Lung Neoplasms 27302168 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-196b reexpression also significantly reduced the growth of tumor xenografts. genetics_overexpression_suppress hsa-mir-200c Lung Neoplasms 25277203 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-200c overexpression is associated with better efficacy of EGFR-TKIs in non-small cell lung cancer patients with EGFR wild-type. genetics_overexpression_suppress hsa-mir-200c Lung Neoplasms 27432063 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Over expression of miR-200c could significantly inhibit cell proliferation, induce G0/G1 cell cycle arrest and induce cell apoptosis. genetics_overexpression_suppress hsa-mir-338 Lung Neoplasms 27431198 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Regaining the expression of miR-338 in lung cancer cell lines significantly impaired cellular adhesion, migration, invasion and lung tumor formation in nude mice. genetics_overexpression_suppress hsa-mir-34a Lung Neoplasms 27109632 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Systemic and local injection of ghR-form miR-34a (ghR-34a) suppressed tumor growth in a mouse model of RAS-induced lung cancer. genetics_overexpression_suppress hsa-mir-34c Lung Neoplasms 19228723 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-34c: were repressed, overexpression can inhibitu lung cancer growth genetics_overexpression_suppress hsa-mir-450 Lung Neoplasms 27246609 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 transfection with lentivirus carrying miR鈥?50 upregulated miR鈥?50 expression and significantly attenuated lung cancer cell proliferation and invasion genetics_overexpression_suppress hsa-mir-7 Lung Neoplasms 25334070 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Restoration of miR-7 inhibited 3LL cell proliferation, induced cell apoptosis in vitro and reduced tumorigenicity in vivo. genetics_overexpression_suppress hsa-mir-130b Lupus Nephritis 27111096 urinary system disease DOID:0080162 M32.14 D008181 overexpressing miR-130b suppressed signaling downstream from the type I IFN pathway in RMCs by targeting IFN regulatory factor 1 (IRF-1). genetics_overexpression_suppress hsa-mir-520a Lymphoma 27461820 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 Our data indicated that the mimics of miR鈥?20a inhibited growth, proliferation of Raji cells and promoted its apoptosis, which was related to downregulation of AKT1, NF鈥懳築 and ER stress response mediated by PERK/eIF2伪 pathway. genetics_overexpression_suppress hsa-mir-520a Lymphoma, Burkitt 27461820 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 Our data indicated that the mimics of miR鈥?20a inhibited growth, proliferation of Raji cells and promoted its apoptosis, which was related to downregulation of AKT1, NF鈥懳築 and ER stress response mediated by PERK/eIF2伪 pathway. genetics_overexpression_suppress hsa-mir-24 Lymphoma, Hodgkin 28432871 disease of cellular proliferation DOID:8567 C81 D006689 236000 HP:0012189 miR-24-3p Is Overexpressed in Hodgkin Lymphoma and Protects Hodgkin and Reed-Sternberg Cells from Apoptosis. genetics_overexpression_suppress hsa-mir-520a Lymphoma, Hodgkin 27461820 disease of cellular proliferation DOID:8567 C81 D006689 236000 HP:0012189 Our data indicated that the mimics of miR鈥?20a inhibited growth, proliferation of Raji cells and promoted its apoptosis, which was related to downregulation of AKT1, NF鈥懳築 and ER stress response mediated by PERK/eIF2伪 pathway. genetics_overexpression_suppress hsa-mir-144 Lymphoma, Large B-Cell 26865454 C83.3 D016403 109565 forced expression of miR-144 significantly attenuated cell proliferation and invasion of OCI-Ly3 cells in vitro, and the tumor-suppressor effect of miR-144 was also confirmed using a xenograft mouse model in vivo Taken together genetics_overexpression_suppress hsa-mir-181a Lymphoma, Large B-Cell 26941399 C83.3 D016403 109565 miR-181a decreases DLBCL tumor cell proliferation and survival, and anti-miR-181a abrogates these effects. genetics_overexpression_suppress hsa-mir-16 Lymphoma, Non-Hodgkin 26640145 disease of cellular proliferation DOID:0060060 C85.9 D008228 605027 HP:0012539 The miR-16 transfection significantly decreased senescent cells and increased apoptotic cells genetics_overexpression_suppress hsa-mir-520a Lymphoma, Non-Hodgkin 27461820 disease of cellular proliferation DOID:0060060 C85.9 D008228 605027 HP:0012539 Our data indicated that the mimics of miR鈥?20a inhibited growth, proliferation of Raji cells and promoted its apoptosis, which was related to downregulation of AKT1, NF鈥懳築 and ER stress response mediated by PERK/eIF2伪 pathway. genetics_overexpression_suppress hsa-mir-16 Lymphoma, T-Cell, Cutaneous 26640145 disease of cellular proliferation DOID:0060061 C84.A0 D016410 608856 HP:0012192 The miR-16 transfection significantly decreased senescent cells and increased apoptotic cells genetics_overexpression_suppress hsa-mir-145 Malignant Neoplasms [unspecific] 25926306 C80.1 D009369 cell proliferation level of OS-732 with microRNA-145 overexpression was significantly decreased, and OS-732 cell invasion capacity was also significantly decreased genetics_overexpression_suppress hsa-mir-124 Medulloblastoma 23172372 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 MiR-124 overexpression inhibits the proliferation of medulloblastoma cells, and this effect is mediated mostly through the action of miR-124 upon CDK6. genetics_overexpression_suppress hsa-mir-129 Medulloblastoma 24093088 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 Overexpression of miR-129-5p using mimics decreased DAOY proliferation genetics_overexpression_suppress hsa-mir-135a Medulloblastoma 25639612 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 Remarkably, enforced expression of miR-135a in HT CSCs strongly inhibited tumorigenesis by repressing the miR-135a direct target gene Arhgef6. genetics_overexpression_suppress hsa-mir-206 Medulloblastoma 25859932 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 MiR-206, a Cerebellum Enriched miRNA Is Downregulated in All Medulloblastoma Subgroups and Its Overexpression Is Necessary for Growth Inhibition of Medulloblastoma Cells. genetics_overexpression_suppress hsa-mir-125b Melanoma 26596831 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Restored expression of miR-125b in melanoma suppressed cell proliferation and invasion both in vitro and in vivo. genetics_overexpression_suppress hsa-mir-137 Melanoma 26186482 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 overexpression of miR-137 inhibited the proliferation of melanoma cells genetics_overexpression_suppress hsa-mir-137 Melanoma 27233613 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Overexpression of miR-137 decreased cell proliferation and colony formation in vitro. genetics_overexpression_suppress hsa-mir-145 Melanoma 24248543 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Overexpression of miR-145 increases the sensitivity of vemurafenib in drug-resistant colo205 cell line. genetics_overexpression_suppress hsa-mir-148b Melanoma 27328731 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Depleting miR-214 or elevating miR-148b blocked the dissemination of melanoma or breast cancer cells, an effect that could be accentuated by dual alteration. genetics_overexpression_suppress hsa-mir-15a Melanoma 27492455 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 miR-15a displayed inhibitory effects on proliferation and invasiveness of several malignant melanoma cell lines. genetics_overexpression_suppress hsa-mir-17 Melanoma 25594054 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 The melanoma tumors formed in mice overexpressing miR-17 were less than that in wild type mice. In addition, the miR-17 tumors were less invasive and less angiogenic. genetics_overexpression_suppress hsa-mir-18b Melanoma 27220837 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Ectopic expression of miR-18b decreased the proliferation of A375 and B16 cells genetics_overexpression_suppress hsa-mir-200c Melanoma 24120113 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Overexpression of microRna-200c in CD44+CD133+ CSCS inhibits the cellular migratory and invasion as well as tumorigenicity in mice. genetics_overexpression_suppress hsa-mir-34a Melanoma 22969970 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 These results suggest that overexpression of miR-34a and c suppresses invasive and generative potentials, respectively, in human malignant melanoma. genetics_overexpression_suppress hsa-mir-34c Melanoma 22969970 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 All four melanoma cell lines showed significant expression of miR-34s - A375: miR-34a 0.6176, miR-34b 0.7625, miR-34c 0.7877; genetics_overexpression_suppress hsa-mir-542 Melanoma 27107696 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Exogenous expression of miR-542-3p resulted in marked inhibition of melanoma cell migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and lung metastasis in vivo. genetics_overexpression_suppress hsa-mir-17 Mesothelioma 27245839 disease of cellular proliferation DOID:1790 C45.9 C562839 156240 HP:0100001 Transfection of MPM cells with a miR-17-5p mimic or KCNMA1-specific siRNAs reduced mRNA expression of KCa1.1 and inhibited MPM cell migration. genetics_overexpression_suppress hsa-mir-202 Multiple Myeloma 25971527 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 The growth rate of miR-202 mimics transfection cells was significantly lower than that of non-transfected cells. genetics_overexpression_suppress hsa-mir-29a Multiple Myeloma 26771839 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 In addition, ectopic expression of miRNA-29a or exposure to PRIMA-1Met reduced cell proliferation and induced apoptosis in MM cells. genetics_overexpression_suppress hsa-mir-206 Muscle Atrophy 27054781 M62.5 D009133 HP:0100295 Injection of miR-206 (30 渭g/rat) attenuated morphological and physiological deterioration of muscle characteristics genetics_overexpression_suppress hsa-mir-1 Myocardial Infarction 26380976 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 miR-1 and -21 jointly blocked hypoxia-induced cardiomyocytes apoptosis. genetics_overexpression_suppress hsa-mir-133a Myocardial Infarction 25465869 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. genetics_overexpression_suppress hsa-mir-150 Myocardial Infarction 25466411 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 In vivo studies showed that overexpression of miR-150 in mice resulted in improved cardiac function, reduced myocardial infarction size, inhibition of apoptosis, and reduced inflammatory Ly-6C(high) monocyte invasion levels after AMI. genetics_overexpression_suppress hsa-mir-208b Myocardial Infarction 27236543 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 Overexpressing miR-208b improved myocardial functions genetics_overexpression_suppress hsa-mir-21 Myocardial Infarction 25809568 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 In miR-21 group, myocardial infarct size reduced by 36.9% in comparison with LV-GFP group. genetics_overexpression_suppress hsa-mir-21 Myocardial Infarction 26380976 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 miR-1 and -21 jointly blocked hypoxia-induced cardiomyocytes apoptosis. genetics_overexpression_suppress hsa-mir-499 Myocardial Infarction 24646523 cardiovascular system disease DOID:5844 I21 D009203 608557 HP:0001658 We report that cardiac-abundant miR-499 could protect neonatal rat cardiomyocytes against H 2O 2-induced apoptosis. Increased miR-499 level favored survival, while decreased miR-499 level favored apoptosis. genetics_overexpression_suppress hsa-let-7b Myocardial Ischemic-Reperfusion Injury 26542107 D015428 intramyocardial injection of let-7b-modified MSCs significantly enhanced ventricular function and facilitated myocardial repair by protecting transplanted cells from apoptosis and autophagy in the rat cardiac ischemia-reperfusion model. genetics_overexpression_suppress hsa-mir-19b Myocardial Ischemic-Reperfusion Injury 26918829 D015428 we found that overexpression of miR-19b decreased H2O2-induced apoptosis and improved cell survival genetics_overexpression_suppress hsa-mir-613 Myocardial Ischemic-Reperfusion Injury 27534371 D015428 miR-613 inhibits I/R-induced cardiomyocyte apoptosis by targeting PDCD10 by regulating the PI3K/AKT signaling pathway. genetics_overexpression_suppress hsa-let-7 Neoplasms [unspecific] 25597880 C80.1 D009369 let-7 microRNA would be involved in over-expression of cofilin-1 mediated tumor suppression in vitro and in vivo. genetics_overexpression_suppress hsa-let-7 Neoplasms [unspecific] 27295554 C80.1 D009369 genetic rescue of Let-7 miRNA activity in Dicer1-deficient TAMs partly restored their M2-like phenotype and decreased tumour-infiltrating CTLs. genetics_overexpression_suppress hsa-let-7a Neoplasms [unspecific] 24100239 C80.1 D009369 Human Argonaute-3 specifically enhances the passenger strand expression and activity of the tumor suppressor microRNA let-7a. genetics_overexpression_suppress hsa-mir-23b Neoplasms [unspecific] 26198058 C80.1 D009369 miR-23b, miR-199a, and miR-15a displayed increased expression during early AVC development whereas others such as miR-130a and miR-200a display decreased expression levels genetics_overexpression_suppress hsa-mir-26a Nervous System Diseases [unspecific] 25808510 C72.9 D009422 We found that miR-26a up-regulation promoted neurite outgrowth and reduced apoptosis in bupivacaine-injured DRG neurons. genetics_overexpression_suppress hsa-mir-138-1 Neuroblastoma 23562653 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 miR-138 Overexpression is more powerful than hTERT knockdown to potentiate apigenin for apoptosis in neuroblastoma in vitro and in vivo genetics_overexpression_suppress hsa-mir-138-2 Neuroblastoma 23562653 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 miR-138 Overexpression is more powerful than hTERT knockdown to potentiate apigenin for apoptosis in neuroblastoma in vitro and in vivo genetics_overexpression_suppress hsa-mir-141 Neuroblastoma 26936280 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 lentivirus-induced miR-141 upregulation inhibited cancer proliferation, cell cycle progression, migration and increased cisplatin chemosensitivity in vitro. genetics_overexpression_suppress hsa-mir-7 Neurodegenerative Diseases [unspecific] 25071443 D019636 HP:0002180 Overexpression of miR-7 or miR-153 by adenoviral transduction protected cortical neurons from MPP(+)-induced toxicity, restored neuronal viability and anti-apoptotic BCL-2 protein levels while attenuated activation of caspase-3. genetics_overexpression_suppress hsa-mir-98 Neuroinflammation 26126865 Overexpression of let-7 and miR-98 in vitro and in vivo resulted in reduced leukocyte adhesion to and migration across endothelium, diminished expression of pro-inflammatory cytokines, and increased BBB tightness, attenuating barrier 'leakiness' in neuroinflammation conditions. genetics_overexpression_suppress hsa-mir-183 Neuropathic Pain 24612023 D009437 Intrathecal administration of lentivirions expressing miR-183 downregulated SNL-induced increases in the expression of Nav1.3 and brain-derived neurotrophic factor (BDNF), which correlated with the significant attenuation of SNL-induced mechanical allodynia. genetics_overexpression_suppress hsa-mir-221 Neuropathic Pain 27059231 D009437 Intrathecal injection of a miR-221 inhibitor attenuated CCI-induced mechanical allodynia and thermal hyperalgesia, and reduced proinflammatory cytokine expression genetics_overexpression_suppress hsa-mir-210 Osteoarthritis 26244598 musculoskeletal system disease DOID:8398 M19.9 D010003 165720 HP:0002758 Transfection with miR-210 mimic inhibited LPS-induced pro-inflammatory cytokines production, cell viability reduction and cell apoptosis. genetics_overexpression_suppress hsa-mir-222 Osteoarthritis 26673737 musculoskeletal system disease DOID:8398 M19.9 D010003 165720 HP:0002758 Over-expression of miR-222 significantly suppressed apoptotic death by down-regulating HDAC-4 and MMP-13 level. genetics_overexpression_suppress hsa-mir-23a Osteoarthritis 27318087 musculoskeletal system disease DOID:8398 M19.9 D010003 165720 HP:0002758 miR-23a-3p overexpression suppresses type II collagen and aggrecan expression genetics_overexpression_suppress hsa-let-7g Osteosarcoma 25197332 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Functional investigation revealed both restoration of let-7g and silencing Aurora-B induce cell apoptosis and suppressed cell viability, migratory and invasive ability in OS cells. genetics_overexpression_suppress hsa-mir-100 Osteosarcoma 26018508 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Overexpression of miR-100 inhibits growth of osteosarcoma through FGFR3. genetics_overexpression_suppress hsa-mir-101 Osteosarcoma 27073439 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Independent inhibition of c-FOS and overexpression of miR-101 expression levels significantly suppressed U2OS cell proliferation, migration and invasion (P<0.01). genetics_overexpression_suppress hsa-mir-106a Osteosarcoma 27383537 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Downregulation of miR-106a-5p was found in OS tissues, and upregulation of miR-106a-5p can inhibit the proliferation, migration, and invasion by targeting HMGA2 in OS cells. genetics_overexpression_suppress hsa-mir-124 Osteosarcoma 25667613 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 transfection of miR-124 mimic into MG63 cells was able to reduce cell proliferation, invasion and migration, and promote cell apoptosis. genetics_overexpression_suppress hsa-mir-125b Osteosarcoma 26744308 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 stable overexpression of miR-125b in osteosarcoma cell lines U2OS and MG-63 inhibited cell proliferation, migration, and invasion. genetics_overexpression_suppress hsa-mir-138 Osteosarcoma 27095063 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 miR-138 inhibited cell proliferation and invasion, and promoted cell apoptosis of human osteosarcoma cells. genetics_overexpression_suppress hsa-mir-140 Osteosarcoma 26219893 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 relative miR-140 expression was increased, cell proliferation was inhibited, cell population in G0/G1 phase was increased, cell population in G2/M phase and S phases and proliferation index (PI), and cell migration distance were decreased in the miR-140 mimic group genetics_overexpression_suppress hsa-mir-140 Osteosarcoma 27624383 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Overexpression of miR-140 Inhibits Proliferation of Osteosarcoma Cells via Suppression of Histone Deacetylase 4. genetics_overexpression_suppress hsa-mir-143 Osteosarcoma 25576341 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Forced miR-143 expression significantly inhibited tumor growth in xenograft SAOS-2-Dox and U2OS-Dox animal models. genetics_overexpression_suppress hsa-mir-150 Osteosarcoma 26561465 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 restoration of miR-150 expression in OS cells could inhibit cell proliferation, migration, and invasion and induced apoptosis in vitro as well as suppressed tumor growth of OS in vivo. genetics_overexpression_suppress hsa-mir-182 Osteosarcoma 27123060 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 upregulation of miRNA-182 promotes cell apoptosis and inhibits cell viability, proliferation, invasion and migration. genetics_overexpression_suppress hsa-mir-224 Osteosarcoma 27222381 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 overexpression of miR-224 suppressed osteosarcoma cell proliferation, migration and invasion genetics_overexpression_suppress hsa-mir-26a Osteosarcoma 27270422 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 miR-26a overexpression inhibits the tumor cell growth both in vitro and in vivo. genetics_overexpression_suppress hsa-mir-26a Osteosarcoma 27468358 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Using in vitro and in vivo assays, we confirmed that miR-26a could inhibit the abilities of in vitro proliferation and suppress in vivo tumor growth in mouse model. genetics_overexpression_suppress hsa-mir-329 Osteosarcoma 27487475 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 MiR-329 is able to inhibit osteosarcoma cell proliferation, promote apoptosis, and induce G0/G1 cell cycle arrest. genetics_overexpression_suppress hsa-mir-34b Osteosarcoma 26924291 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Upregulation of miR-34b also induced apoptosis and increased the sensitivity of the cells to the anticancer drugs genetics_overexpression_suppress hsa-mir-422a Osteosarcoma 27779704 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Overexpression of miR-422a inhibits cell proliferation and invasion, and enhances chemosensitivity in osteosarcoma cells. genetics_overexpression_suppress hsa-mir-497 Osteosarcoma 27176490 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 upregulation of miR鈥?97 inhibited cell proliferation, migration and invasion in osteosarcoma cell lines genetics_overexpression_suppress hsa-mir-503 Osteosarcoma 26768615 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 miR-503 overexpression suppressed cell invasion and migration and inhibited epithelial-to-mesenchymal transition (EMT) of MG-63. genetics_overexpression_suppress hsa-let-7c Ovarian Neoplasms 24507678 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 After application of let-7c, number of T29A2+ cell clones was decreased significantly, however, after the application of Anti-let-7, the number of clones restored, and there was no significant difference compared with the negative control group. genetics_overexpression_suppress hsa-mir-100 Ovarian Neoplasms 26607088 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 The expression of miR-100 is downregulated in SKOV3/DDP cells.Overexpressing miR-100 may effectively increase the sensitivity to cisplatin of human ovarian epithelial cancer SKOV3/DDP cells and may reverse cisplatin-resistance of EOC (epithelial ovarian cancer). genetics_overexpression_suppress hsa-mir-100 Ovarian Neoplasms 20081105 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Overexpression of mir-100 inhibited mTOR signaling and enhanced sensitivity to the rapamycin analog RAD001 (everolimus), confirming the key relationship between mir-100 and the mTOR pathway. genetics_overexpression_suppress hsa-mir-125b Ovarian Neoplasms 27383536 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Ectopic expression of miR-125b in EOC cells significantly inhibited tumor invasion. genetics_overexpression_suppress hsa-mir-130b Ovarian Neoplasms 27048832 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 overexpression of miR-130b reduced the expression of RUNX3 and inhibited cancer cell migration and invasion of EOC cells genetics_overexpression_suppress hsa-mir-145 Ovarian Neoplasms 27191261 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Activating miR-145 suppresses ovarian tumor growth and metastasis genetics_overexpression_suppress hsa-mir-155 Ovarian Neoplasms 23523916 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 overexpression of miR-155 may prevent tumorigenesis in human ovarian cancer through downregulation of CLDN1. genetics_overexpression_suppress hsa-mir-206 Ovarian Neoplasms 24604205 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 microRNA-206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α-positive ovarian cancer cells. genetics_overexpression_suppress hsa-mir-215 Ovarian Neoplasms 26676658 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Upregulation of miR-215 inhibited cell proliferation, promoted apoptosis and increased sensitivity to chemotherapy drugs in EOC cells. genetics_overexpression_suppress hsa-mir-22 Ovarian Neoplasms 20081105 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 overexpression of the putative tumor suppressor mir-22 repressed the EVI1 oncogene, which is known to suppress apoptosis by stimulating phosphatidylinositol 3-kinase/v-akt murine thymoma viral oncogene homolog 1 signaling. genetics_overexpression_suppress hsa-mir-26a Ovarian Neoplasms 27158389 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 over-expression could significantly inhibit the proliferation of ovarian cancer cells and induce their apoptosis. genetics_overexpression_suppress hsa-mir-29a Ovarian Neoplasms 22479643 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 over-expression of miR-29a in vitro repressed several anti-correlated genes (including DNMT3A and DNMT3B) and substantially decreased ovarian cancer cell viability. genetics_overexpression_suppress hsa-mir-338 Ovarian Neoplasms 27508048 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Restoration of miR-338-3p expression in ovarian cancer cells could inhibit cell proliferation, lactate production and lactate production of ovarian cancer cells. genetics_overexpression_suppress hsa-mir-381 Ovarian Neoplasms 26768613 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Overexpression of miR-381 significantly inhibited EOC cell proliferation, migration, and invasion. genetics_overexpression_suppress hsa-mir-494 Ovarian Neoplasms 27313773 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Overexpression of miR-494 inhibited ovarian cancer cell proliferation by inducing apoptosis. genetics_overexpression_suppress hsa-let-7 Pancreatic Neoplasms 25017900 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Sulforaphane, quercetin and catechins complement each other in elimination of advanced pancreatic cancer by miR-let-7 induction and K-ras inhibition. genetics_overexpression_suppress hsa-mir-506 Pancreatic Neoplasms 27065335 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 miR-506 inhibited cell proliferation, induced cell cycle arrest at the G1/S transition and enhanced apoptosis and chemosensitivity of pancreatic cancer cells. genetics_overexpression_suppress hsa-mir-548an Pancreatic Neoplasms 27353169 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 overexpression of miR-548an significantly inhibited the proliferation and invasion of pancreatic cancer cell genetics_overexpression_suppress hsa-mir-7 Parkinson Disease 27003614 nervous system disease DOID:14330 G20 D010300 PS168600 The upregulation of miR-7 promoted cell viability and suppressed cell apoptosis in MPP(+)-treated SH-SY5Y cells. genetics_overexpression_suppress hsa-mir-132 Prostate Neoplasms 27527117 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Notably, overexpression of miR-132/212 could inhibit TGF-β (transforming growth factor-β)-induced EMT in Vcap and Lncap cells at both the mRNA and protein expression levels. genetics_overexpression_suppress hsa-mir-143 Prostate Neoplasms 26269764 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-143 has an inhibitory effect on cell proliferation as evidenced by decreased cell viability, increased cell apoptosis and cell cycle arrest at the G1/S transition. genetics_overexpression_suppress hsa-mir-143 Prostate Neoplasms 26721309 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-143 restoration decreased secreted MMP-2 and MMP-9 enzyme activities compared with scramble controls genetics_overexpression_suppress hsa-mir-145 Prostate Neoplasms 25951106 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Overexpression of miR-145-5p inhibits proliferation of prostate cancer cells and reduces SOX2 expression. genetics_overexpression_suppress hsa-mir-154 Prostate Neoplasms 27074041 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The forced expression of miR-154-5p or E2F5 knockdown significantly restrained cell growth, as well as the migratory and invasive capabilities. genetics_overexpression_suppress hsa-mir-195 Prostate Neoplasms 27175617 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-195 overexpression inhibited cell proliferation, cell cycle progression and tumorigenesis via directly targeting HMGA1. genetics_overexpression_suppress hsa-mir-23b Prostate Neoplasms 26898757 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-23b/-27b expression in prostate cancer cells decreased seminal vesicle invasion and distant metastases genetics_overexpression_suppress hsa-mir-26a Prostate Neoplasms 27449037 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 It was confirmed that miR-26a-5p was markedly downregulated in PC tissues compared with normal controls whose reduced expression was significantly associated with metastasis and poor overall prognosis and found that miR-26a-5p was able to prevent proliferation and motility of PC cells in vitro. genetics_overexpression_suppress hsa-mir-27b Prostate Neoplasms 26898757 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-23b/-27b expression in prostate cancer cells decreased seminal vesicle invasion and distant metastases genetics_overexpression_suppress hsa-mir-29a Prostate Neoplasms 26131109 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 enforced expression of miR-29a in PC-3 and LNCaP cells inhibited proliferation, and induced apoptosis by repressing the expression of KDM5B. genetics_overexpression_suppress hsa-mir-29b Prostate Neoplasms 25784815 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 forced expression of miR-29b inhibited cell proliferation and cell invasion and induced cell apoptosis in PCa. genetics_overexpression_suppress hsa-mir-30a Prostate Neoplasms 27431942 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR鈥?0a overexpression resulted in a significant suppression of cell growth in vitro, and reduced tumorigenicity in vivo. genetics_overexpression_suppress hsa-mir-320 Prostate Neoplasms 27216188 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 An miR-320a mimic suppressed AR protein expression together with growth suppression genetics_overexpression_suppress hsa-mir-320a Prostate Neoplasms 27212625 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Restoration of mature miR鈥?20a in PCa cell lines showed that miR鈥?20a significantly inhibited cancer cell migration and invasion. genetics_overexpression_suppress hsa-mir-34a Prostate Neoplasms 26722316 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The over-expression of miR-34a inhibited PC-3 cells growth and resulted in increased cell cycle arrest compared with the negative control (P<0.05). genetics_overexpression_suppress hsa-mir-34c Prostate Neoplasms 27461446 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 In this study, we identified that miR-34C was under-expressed in the purified CD133+ PCSCs and enforced introduction of miR-34C attenuated the stemness of CD133+ PCSCs. genetics_overexpression_suppress hsa-mir-449a Prostate Neoplasms 26520443 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Overexpression of miR-449a induces cell cycle arrest, apoptosis, and senescence genetics_overexpression_suppress hsa-mir-34 Pulmonary Hypertension 27302634 cardiovascular system disease DOID:6432 I27.20 D006976 PS178600 HP:0002092 miR-34a overexpression down-regulated platelet-derived growth factor receptor alpha (PDGFRA) expression, which is a key factor in PAH development. genetics_overexpression_suppress hsa-mir-184 Retinal Neovascularization 25796186 H35.059 D015861 HP:0030666 miR-184 mimic inhibits Wnt signaling in the OIR retina genetics_overexpression_suppress hsa-mir-124 Retinoblastoma 27498908 nervous system disease DOID:768 C69.20 D012175 180200 HP:0009919 The ectopic expression of miR-124 in the RB cell lines (Y79 and SO-RB50) suppresses cell proliferation, migration and invasion, induced cell apoptosis in vitro. genetics_overexpression_suppress hsa-mir-125a Retinoblastoma 27094723 nervous system disease DOID:768 C69.20 D012175 180200 HP:0009919 The overexpression of miR-125a-5p significantly suppressed cell proliferation and tumor formation in retinoblastoma. genetics_overexpression_suppress hsa-mir-140 Rheumatoid Arthritis 26473405 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Overexpression of miRNAs 140-3p and 140-5p caused a reduction in expression, with correlated kinetic patterns, of their corresponding target molecules sirtuin 1 and stromal cell-derived factor 1 in the SFs and joints of mice. genetics_overexpression_suppress hsa-mir-17 Rheumatoid Arthritis 27534557 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 MicroRNA-17 Suppresses TNF-B Signaling by Interfering with TRAF2 and cIAP2 Association in Rheumatoid Arthritis Synovial Fibroblasts. genetics_overexpression_suppress hsa-mir-223 Rheumatoid Arthritis 22903258 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Overexpression of microRNA-223 in rheumatoid arthritis synovium controls osteoclast differentiation. genetics_overexpression_suppress hsa-mir-451 Rheumatoid Arthritis 26823778 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 miR-451 treatment significantly decreased cell proliferation ability genetics_overexpression_suppress hsa-mir-573 Rheumatoid Arthritis 26166764 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 miR-573 overexpression suppressed the expression of interleukin 6 (IL-6) and cyclooxygenase 2 in RASFs genetics_overexpression_suppress hsa-mir-16 Sarcoma [unspecific] 26044957 disease of cellular proliferation DOID:1115 C49 D012509 HP:0100242 miR-16, but not other downregulated miRNAs, was able to significantly suppress both migration and invasion in vitro genetics_overexpression_suppress hsa-mir-9 Schizophrenia 27117414 disease of mental health DOID:5419 F20 D012559 181500 HP:0100753 Overexpression of miR-9 was sufficient to ameliorate a previously reported neural migration deficit in SZ NPCs, whereas knockdown partially phenocopied aberrant migration in control NPCs. genetics_overexpression_suppress hsa-mir-146a Sepsis 26048146 A41.9 D018805 HP:0100806 In vivo transfection of LmiR-146a attenuated sepsis-induced cardiac dysfunction. genetics_overexpression_suppress hsa-mir-146a Sepsis 26138422 A41.9 D018805 HP:0100806 Up-regulation of miR-146a inhibit the release of the inflammatory cytokine TNF-伪 stimulated by sepsis, and alleviate inflammatory reaction and lung tissue injury in mice with sepsis-induced ALI. genetics_overexpression_suppress hsa-mir-126 Spinal Cord Injuries 25724143 S34.139A D013119 increased levels of miR-126 promoted angiogenesis, and inhibited leukocyte extravasation into the injured spinal cord genetics_overexpression_suppress hsa-mir-9 Spinal Cord Injuries 26359086 S34.139A D013119 miR-9 overexpression promoted osteoblast differentiation and angiogenesis genetics_overexpression_suppress hsa-mir-1 Squamous Cell Carcinoma, Esophageal 25672418 disease of cellular proliferation DOID:3748 C562729 Downregulation of microRNA-1 in esophageal squamous cell carcinoma correlates with an advanced clinical stage and its overexpression inhibits cell migration and invasion. genetics_overexpression_suppress hsa-mir-1 Squamous Cell Carcinoma, Esophageal 27247259 disease of cellular proliferation DOID:3748 C562729 miR鈥? suppressed ESCC cell proliferation and increased apoptosis genetics_overexpression_suppress hsa-mir-143 Squamous Cell Carcinoma, Esophageal 26758433 disease of cellular proliferation DOID:3748 C562729 miR-143 exerted a tumor-suppressing effect by inhibiting the proliferation, migration, and invasion and inducing G1/G0 phase arrest of ESCC cells via the negative regulation of FAM83F expression. genetics_overexpression_suppress hsa-mir-143 Squamous Cell Carcinoma, Esophageal 27358073 disease of cellular proliferation DOID:3748 C562729 Ectopic expression of miR-143-3p also reduced the metastatic potential of cells by selectively regulating epithelial-mesenchymal transition regulatory proteins. genetics_overexpression_suppress hsa-mir-194 Squamous Cell Carcinoma, Esophageal 27480251 disease of cellular proliferation DOID:3748 C562729 miR-194 was found to inhibit proliferation and invasion and promote apoptosis of esophageal squamous cell carcinoma cells. genetics_overexpression_suppress hsa-mir-20a Squamous Cell Carcinoma, Esophageal 27508097 disease of cellular proliferation DOID:3748 C562729 Together, our findings demonstrate that miR-17/20a suppresses cell migration and invasion of ESCC by modulating TGF-尾/ITGB6 pathway. genetics_overexpression_suppress hsa-mir-622 Squamous Cell Carcinoma, Esophageal 27501502 disease of cellular proliferation DOID:3748 C562729 Up-regulation of miR-622 could significantly reduce ESCC cell proliferation, enhance cell apoptosis, and impair cell invasion and migration in vitro, while down-regulation of miR-622 showed opposite effects. genetics_overexpression_suppress hsa-mir-1 Squamous Cell Carcinoma, Head and Neck 27169691 disease of cellular proliferation DOID:5520 C76.0 C535575 miR-1 and miR-206 significantly inhibited HNSCC cells' aggressiveness. genetics_overexpression_suppress hsa-mir-203 Squamous Cell Carcinoma, Head and Neck 26882562 disease of cellular proliferation DOID:5520 C76.0 C535575 oreover, ectopic overexpression of miR-203 suppressed the invasion and induced mesenchymal-epithelial transition (MET) in HNSCC cells. genetics_overexpression_suppress hsa-mir-206 Squamous Cell Carcinoma, Head and Neck 27169691 disease of cellular proliferation DOID:5520 C76.0 C535575 restoration of miR-1 and miR-206 significantly inhibited HNSCC cells' aggressiveness. genetics_overexpression_suppress hsa-mir-149 Squamous Cell Carcinoma, Laryngeal or Hypopharyngeal 27403438 disease of cellular proliferation DOID:2876 In vitro studies revealed that the exogenous expression of miRNA-149 inhibits the proliferation of human Hep-2 cells and induces cell apoptosis. genetics_overexpression_suppress hsa-mir-34a Squamous Cell Carcinoma, Laryngeal or Hypopharyngeal 24482044 disease of cellular proliferation DOID:2876 Ectopic expression of miR-34a and miR-34c in Hep-2 cells significantly induced the cell proliferation and migration ability in vitro. genetics_overexpression_suppress hsa-mir-34c Squamous Cell Carcinoma, Laryngeal or Hypopharyngeal 24482044 disease of cellular proliferation DOID:2876 Ectopic expression of miR-34a and miR-34c in Hep-2 cells significantly induced the cell proliferation and migration ability in vitro. genetics_overexpression_suppress hsa-mir-375 Squamous Cell Carcinoma, Laryngeal or Hypopharyngeal 27279635 disease of cellular proliferation DOID:2876 Overexpression of miR-375 led to a decreased protein level of Kr眉ppel-like factor 4 (KLF4) and marked suppression of the proliferation and invasion, and induced apoptosis of LSCC cell line genetics_overexpression_suppress hsa-mir-181d Squamous Cell Carcinoma, Oral 26693182 disease of cellular proliferation DOID:0050866 Ectopic expression of miR-181a/d decreased anchorage independent growth and CSC phenotype of HPV16-transfected OSCC. genetics_overexpression_suppress hsa-mir-206 Squamous Cell Carcinoma, Oral 25246801 disease of cellular proliferation DOID:0050866 upregulation of miR-206 in Tca8113 cells was able to reduce cell proliferation, invasion, and migration and promote cell apoptosis in vitro. genetics_overexpression_suppress hsa-mir-20a Squamous Cell Carcinoma, Oral 26781875 disease of cellular proliferation DOID:0050866 Upregulation of miR-20a by transfected plasmid HPV-16 E7 can significantly inhibit Cal27 cell proliferation, invasion, and migration. genetics_overexpression_suppress hsa-mir-27a Squamous Cell Carcinoma, Oral 27432214 disease of cellular proliferation DOID:0050866 Intriguingly, increased expression of miR-27a-3p could significantly decrease the expression level of YAP1 as well as several epithelial to mesenchymal transition (EMT)-related molecules in OSCC cell lines, including Twist and Snail. genetics_overexpression_suppress hsa-mir-448 Squamous Cell Carcinoma, Oral 27184799 disease of cellular proliferation DOID:0050866 Knockdown of N4BP2L1 and upregulation of miR-448 significantly reduced the invasive potential of oral squamous cell carcinoma cells. genetics_overexpression_suppress hsa-mir-222 Squamous Cell Carcinoma, Tongue 26517090 disease of cellular proliferation DOID:0050865 C02.9 Moreover, miR-222 mimics and ABCG2 siRNA inhibited tumor growth and lung metastasis in vivo. genetics_overexpression_suppress hsa-mir-410 Systemic Lupus Erythematosus 27351906 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 overexpression of miR-410 significantly reduced the expression levels of IL-10. genetics_overexpression_suppress hsa-mir-199a Testicular Neoplasms 27432288 disease of cellular proliferation DOID:2998 D013736 273300 HP:0010788 it was determined that overexpression of miR鈥?99a鈥?p in Ntera鈥? cells caused suppression of cell growth and migration. genetics_overexpression_suppress hsa-mir-126 Thyroid Neoplasms 27175968 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 upregulation of miR鈥?26 inhibited cell proliferation, migration and invasion in thyroid cancer cells. genetics_overexpression_suppress hsa-mir-195 Thyroid Neoplasms 26527888 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 exogenous overexpression of miR-195 significantly inhibits the protein expression of Raf1 and blocks the thyroid cancer cell proliferation. genetics_overexpression_suppress hsa-mir-211 Thyroid Neoplasms 28703321 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Overexpression miR-211-5p hinders the proliferation, migration, and invasion of thyroid tumor cells by downregulating SOX11. genetics_overexpression_suppress hsa-let-7b Uveal Melanoma 25588203 C536494 155720 HP:0007716 We then confirmed that let-7b mimics could inhibit UM growth both in vitro and in vivo. genetics_overexpression_suppress hsa-mir-1 Vascular Hypertrophy 26253469 the administration of a miR-1 mimic attenuated cardiac hypertrophy by suppressing the transverse aortic constriction-induced increase in myocardin expression genetics_overexpression_suppress hsa-mir-133a Vascular Hypertrophy 25995211 delivery of miR-1 and miR-133a suppressed inducible cAMP early repressor expression and prevented both electrical remodeling and hypertrophy. genetics_overexpression_suppress hsa-mir-26a Vascular Hypertrophy 27485101 Taken together, the present study suggested an anti鈥慼ypertrophic role of miR鈥?6a in cardiac hypertrophy, possibly via inhibition of GATA4. genetics_overexpression_suppress hsa-mir-29b Wound Healing 27477081 D014945 HP:0001058 Importantly, local delivery of miR-29b lentiviral particles inhibited HSP47 expression and collagen biosynthesis as well as suppressed angiogenesis, thus reducing scar formation in an excisional wound splinting model.