category mir disease pmid root_name doid icd10cm mesh omim hpo description epigenetics hsa-mir-31 Adenocarcinoma, Colon 24752710 disease of cellular proliferation DOID:234 C18 HP:0040276 MicroRNA-31 expression in relation to BRAF mutation, CpG island methylation and colorectal continuum in serrated lesions. epigenetics hsa-mir-106b Adenocarcinoma, Esophageal 28049580 disease of cellular proliferation DOID:4914 C562730 133239 Epigenetic regulation on the gene expression signature in esophagus adenocarcinoma. epigenetics hsa-mir-193b Adenocarcinoma, Esophageal 27176876 disease of cellular proliferation DOID:4914 C562730 133239 Aberrant methylation of microRNA-193b in human Barrett's esophagus and esophageal adenocarcinoma epigenetics hsa-mir-145 Adenocarcinoma, Lung 26582602 disease of cellular proliferation DOID:3910 C78.00 C538231 211980 HP:0030078 Taken together, DNA hyper-methylation in the miR-145 promoter region reduced its expression in LAC and miR-145 expression level might serve as a novel prognostic biomarker. epigenetics hsa-mir-615 Adenocarcinoma, Pancreatic Ductal 24769899 disease of cellular proliferation DOID:3498 C25.3 D021441 260350 miR-615-5p is epigenetically inactivated and functions as a tumor suppressor in pancreatic ductal adenocarcinoma. epigenetics hsa-mir-10a Atherosclerosis 26148682 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Methylation-specific PCR (MSP) confirmed differential CpG methylation of HOXA genes, the ER stress gene ATF4, inflammatory regulator microRNA-10a and ARHGAP25 that encodes a negative regulator of Rho GTPases involved in cytoskeleton remodeling. epigenetics hsa-mir-10b Atherosclerosis 28601079 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 Variability of Methylation Profiles of CpG Sites in microrNA Genes in Leukocytes and Vascular Tissues of Patients with Atherosclerosis. epigenetics hsa-mir-152 Atherosclerosis 22295098 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 MicroRNA-152 mediates DNMT1-regulated DNA methylation in the estrogen receptor α gene. epigenetics hsa-mir-29b-1 Atherosclerosis 21266537 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 OxLDL up-regulates microRNA-29b, leading to epigenetic modifications of MMP-2/MMP-9 genes: a novel mechanism for cardiovascular diseases. epigenetics hsa-mir-29b-2 Atherosclerosis 21266537 cardiovascular system disease DOID:1936 I70 D050197 108725 HP:0002621 OxLDL up-regulates microRNA-29b, leading to epigenetic modifications of MMP-2/MMP-9 genes: a novel mechanism for cardiovascular diseases. epigenetics hsa-mir-10a Bladder Neoplasms 23867826 C67 D001749 109800 HP:0009725 Analyses in human urothelial cells identify methylation of miR-152, miR-200b and miR-10a genes as candidate bladder cancer biomarkers. epigenetics hsa-mir-124 Bladder Neoplasms 23200812 C67 D001749 109800 HP:0009725 Among them, miR-137,miR-124-2, miR-124-3, and miR-9-3 were frequently and tumor-specifically methylated in primary cancers epigenetics hsa-mir-137 Bladder Neoplasms 23200812 C67 D001749 109800 HP:0009725 Among them, miR-137,miR-124-2, miR-124-3, and miR-9-3 were frequently and tumor-specifically methylated in primary cancers epigenetics hsa-mir-152 Bladder Neoplasms 23867826 C67 D001749 109800 HP:0009725 Analyses in human urothelial cells identify methylation of miR-152, miR-200b and miR-10a genes as candidate bladder cancer biomarkers. epigenetics hsa-mir-193a Bladder Neoplasms 25188512 C67 D001749 109800 HP:0009725 The DNA methylation-regulated miR-193a-3p dictates the multi-chemoresistance of bladder cancer via repression of SRSF2/PLAU/HIC2 expression. epigenetics hsa-mir-200b Bladder Neoplasms 23867826 C67 D001749 109800 HP:0009725 Analyses in human urothelial cells identify methylation of miR-152, miR-200b and miR-10a genes as candidate bladder cancer biomarkers. epigenetics hsa-mir-34a Bladder Neoplasms 24423412 C67 D001749 109800 HP:0009725 Cisplatin-based chemotherapy induced demethylation of miR-34a promoter and increased miR-34a expression, which in turn sensitized MIBC cells to cisplatin and decreased the tumorigenicity and proliferation of cancer cells that by reducing the production of CD44. epigenetics hsa-mir-34b Bladder Neoplasms 27557899 C67 D001749 109800 HP:0009725 MicroRNA epigenetic signatures in human disease. epigenetics hsa-mir-9 Bladder Neoplasms 23200812 C67 D001749 109800 HP:0009725 Among them, miR-137,miR-124-2, miR-124-3, and miR-9-3 were frequently and tumor-specifically methylated in primary cancers epigenetics hsa-let-7e Breast Neoplasms 21969366 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Jumonji/Arid1 B (JARID1B) promotes breast tumor cell cycle progression through epigenetic repression of micro RNA let-7e. epigenetics hsa-mir-124a-1 Breast Neoplasms 24375250 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Methylation of miR-124a-1, miR-124a-2, and miR-124a-3 genes correlates with aggressive and advanced breast cancer disease. epigenetics hsa-mir-124a-2 Breast Neoplasms 24375250 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Methylation of miR-124a-1, miR-124a-2, and miR-124a-3 genes correlates with aggressive and advanced breast cancer disease. epigenetics hsa-mir-124a-3 Breast Neoplasms 24375250 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Methylation of miR-124a-1, miR-124a-2, and miR-124a-3 genes correlates with aggressive and advanced breast cancer disease. epigenetics hsa-mir-125b-1 Breast Neoplasms 22277129 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 We observed a significant reduction on the expression of miR-125b1 in cancer cells in comparison with controls, suggesting that DNA methylation at the CpG island might reduce miR-125b1 expression. epigenetics hsa-mir-129-2 Breast Neoplasms 26519551 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 In summary, the obtained data indicate the involvement of methylation in the down-regulation of the studied coding and miRNA genes and suggest the involvement of miR-129-2 in the deregulation of RASSF1(A) via a direct interaction or/and mediators in common pathways (according to KEGG, Gene Ontology (FDR < 0.01), and GeneCards data) in the examined gynecological tumors. epigenetics hsa-mir-143 Breast Neoplasms 24218337 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 MicroRNA-143 is downregulated in breast cancer and regulates DNA methyltransferases 3A in breast cancer cells. epigenetics hsa-mir-148a Breast Neoplasms 25980823 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Glabridin inhibits cancer stem cell-like properties of human breast cancer cells:An epigenetic regulation of miR-148a/SMAd2 signaling. epigenetics hsa-mir-148b Breast Neoplasms 24257477 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Our data provide novel evidence of the mechanisms behind miRNA dysregulation in breast cancer. The study contributes to the understanding of how methylation and copy number alterations influence miRNA expression, emphasizing miRNA functionality through redundant encoding, and suggests novel miRNAs important in breast cancer. epigenetics hsa-mir-149 Breast Neoplasms 25156775 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Methylation-regulated miR-149 modulates chemoresistance by targeting GlcNAc N-deacetylase/N-sulfotransferase-1 in human breast cancer. epigenetics hsa-mir-151a Breast Neoplasms 24257477 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Our data provide novel evidence of the mechanisms behind miRNA dysregulation in breast cancer. The study contributes to the understanding of how methylation and copy number alterations influence miRNA expression, emphasizing miRNA functionality through redundant encoding, and suggests novel miRNAs important in breast cancer. epigenetics hsa-mir-199a-1 Breast Neoplasms 21317930 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-199a-2 Breast Neoplasms 21317930 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-199b Breast Neoplasms 21317930 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-19a Breast Neoplasms 27445062 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 CAP treatment of MCF-7 induced hypermethylation at the promoter CpG sites and downregulation of miR-19a, which was known as an oncomiR. epigenetics hsa-mir-200 Breast Neoplasms 24918286 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 SUMOylation of FOXM1B alters its transcriptional activity on regulation of MiR-200 family and JNK1 in MCF7 human breast cancer cells. epigenetics hsa-mir-200 Breast Neoplasms 23525011 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Epigenetic modulation of the miR-200 family is associated with transition to a breast cancer stem cell-like state epigenetics hsa-mir-200a Breast Neoplasms 23112837 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the expression and methylation status of miR-200f could be used as hypothetical biomarkers to assess the occurrence of EMT in breast cancer epigenetics hsa-mir-200b Breast Neoplasms 22231446 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Methylation of functional promoters of the Hsa-mir-200b is associated with metastasis or hormone receptor status in advanced breast cancer. epigenetics hsa-mir-200b Breast Neoplasms 23112837 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the expression and methylation status of miR-200f could be used as hypothetical biomarkers to assess the occurrence of EMT in breast cancer epigenetics hsa-mir-200c Breast Neoplasms 24729530 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Induction of the mesenchymal to epithelial transition by demethylation- activated microRNA-200c is involved in the anti-migration/invasion effects of arsenic trioxide on human breast cancer cells. epigenetics hsa-mir-200c Breast Neoplasms 23112837 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 the expression and methylation status of miR-200f could be used as hypothetical biomarkers to assess the occurrence of EMT in breast cancer epigenetics hsa-mir-200c Breast Neoplasms 28724364 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Tamoxifen reverses epithelial-mesenchymal transition by demethylating miR-200c in triple-negative breast cancer cells. epigenetics hsa-mir-203 Breast Neoplasms 22393463 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Epigenetic Silencing of miR-203 Upregulates SNAI2 and Contributes to the Invasiveness of Malignant Breast Cancer Cells. epigenetics hsa-mir-21 Breast Neoplasms 24257477 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Our data provide novel evidence of the mechanisms behind miRNA dysregulation in breast cancer. The study contributes to the understanding of how methylation and copy number alterations influence miRNA expression, emphasizing miRNA functionality through redundant encoding, and suggests novel miRNAs important in breast cancer. epigenetics hsa-mir-218-1 Breast Neoplasms 22705304 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-7 and miR-218 epigenetically control tumor suppressor genes RASSF1A and Claudin-6 by targeting HoxB3 in breast cancer. epigenetics hsa-mir-218-2 Breast Neoplasms 22705304 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-7 and miR-218 epigenetically control tumor suppressor genes RASSF1A and Claudin-6 by targeting HoxB3 in breast cancer. epigenetics hsa-mir-219 Breast Neoplasms 23813567 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Aberrant DNA methylation of miR-219 promoter in long-term night shiftworkers. epigenetics hsa-mir-221 Breast Neoplasms 21673316 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 TRPS1 targeting by miR-221/222 promotes the epithelial-to-mesenchymal transition in breast cancer. epigenetics hsa-mir-27b Breast Neoplasms 27363334 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 MiR-27b is epigenetically downregulated in tamoxifen resistant breast cancer cells epigenetics hsa-mir-29c Breast Neoplasms 24297604 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Dysregulation of microRNA expression drives aberrant DNA hypermethylation in basal-like breast cancer. epigenetics hsa-mir-29c Breast Neoplasms 26539832 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Molecular Subtype-Specific Expression of MicroRNA-29c in Breast Cancer Is Associated with CpG Dinucleotide Methylation of the Promoter. epigenetics hsa-mir-31 Breast Neoplasms 22289355 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-31 and its host gene lncRNA LOC554202 are regulated by promoter hypermethylation in triple-negative breast cancer. epigenetics hsa-mir-320a Breast Neoplasms 25159093 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 A methylation-based regulatory network for microRNA 320a in chemoresistant breast cancer. epigenetics hsa-mir-328 Breast Neoplasms 23991164 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Methylation patterns in the miR-328 5'-flanking region are involved in the inter-individual difference in BCRP levels in human placenta epigenetics hsa-mir-335 Breast Neoplasms 21289068 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 MicroRNA-335 inhibits tumor reinitiation and is silenced through genetic and epigenetic mechanisms in human breast cancer. epigenetics hsa-mir-34a Breast Neoplasms 21225432 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34a Breast Neoplasms 21317930 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-34a Breast Neoplasms 23292869 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Downregulation of miR-34a in breast tumors is not associated with either p53 mutations or promoter hypermethylation while it correlates with metastasis epigenetics hsa-mir-34b Breast Neoplasms 25398683 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 long-term shiftwork may increase the risk of breast cancer via methylation-based suppression of miR-34b and a consequent reduction in immunomediated anti-tumor capacity and support our previous findings that LAN may induce epigenetic alteration of cancer-relevant microRNAs. epigenetics hsa-mir-34b Breast Neoplasms 21225432 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Breast Neoplasms 21225432 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Breast Neoplasms 22074923 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 MiR-34c down-regulation via DNA methylation promotes self-renewal and epithelial-mesenchymal transition in breast tumor-initiating cells. epigenetics hsa-mir-375 Breast Neoplasms 20978187 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 Epigenetically deregulated microRNA-375 is involved in a positive feedback loop with estrogen receptor alpha in breast cancer cells. epigenetics hsa-mir-7-1 Breast Neoplasms 22705304 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-7 and miR-218 epigenetically control tumor suppressor genes RASSF1A and Claudin-6 by targeting HoxB3 in breast cancer. epigenetics hsa-mir-7-2 Breast Neoplasms 22705304 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-7 and miR-218 epigenetically control tumor suppressor genes RASSF1A and Claudin-6 by targeting HoxB3 in breast cancer. epigenetics hsa-mir-7-3 Breast Neoplasms 22705304 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 miR-7 and miR-218 epigenetically control tumor suppressor genes RASSF1A and Claudin-6 by targeting HoxB3 in breast cancer. epigenetics hsa-mir-9-1 Breast Neoplasms 26519551 thoracic disease DOID:1612 C50 D001943 114480 HP:0100013 In summary, the obtained data indicate the involvement of methylation in the down-regulation of the studied coding and miRNA genes and suggest the involvement of miR-129-2 in the deregulation of RASSF1(A) via a direct interaction or/and mediators in common pathways (according to KEGG, Gene Ontology (FDR < 0.01), and GeneCards data) in the examined gynecological tumors. epigenetics hsa-mir-17 Bronchopulmonary Dysplasia 27694474 P27.1 D001997 our data support a plausible role for epigenetically altered miR-17/92 cluster in the pathogenesis of severe BPD epigenetics hsa-mir-18 Bronchopulmonary Dysplasia 27694474 P27.1 D001997 our data support a plausible role for epigenetically altered miR-17/92 cluster in the pathogenesis of severe BPD epigenetics hsa-mir-19a Bronchopulmonary Dysplasia 27694474 P27.1 D001997 our data support a plausible role for epigenetically altered miR-17/92 cluster in the pathogenesis of severe BPD epigenetics hsa-mir-19b-1 Bronchopulmonary Dysplasia 27694474 P27.1 D001997 our data support a plausible role for epigenetically altered miR-17/92 cluster in the pathogenesis of severe BPD epigenetics hsa-mir-20a Bronchopulmonary Dysplasia 27694474 P27.1 D001997 our data support a plausible role for epigenetically altered miR-17/92 cluster in the pathogenesis of severe BPD epigenetics hsa-mir-92-1 Bronchopulmonary Dysplasia 27694474 P27.1 D001997 our data support a plausible role for epigenetically altered miR-17/92 cluster in the pathogenesis of severe BPD epigenetics hsa-mir-34a Carcinoma, Bladder 27557899 urinary system disease DOID:4007 D09.0 D001749 109800 HP:0002862 MicroRNA epigenetic signatures in human disease. epigenetics hsa-mir-34c Carcinoma, Bladder 27557899 urinary system disease DOID:4007 D09.0 D001749 109800 HP:0002862 MicroRNA epigenetic signatures in human disease. epigenetics hsa-mir-107 Carcinoma, Breast 27830681 D05 D001943 114480 HP:0003002 Novel miRNA genes hypermethylated in breast cancer. epigenetics hsa-mir-124 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-1258 Carcinoma, Breast 27830681 D05 D001943 114480 HP:0003002 Novel miRNA genes hypermethylated in breast cancer. epigenetics hsa-mir-125b Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-127 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-130b Carcinoma, Breast 27830681 D05 D001943 114480 HP:0003002 Novel miRNA genes hypermethylated in breast cancer. epigenetics hsa-mir-132 Carcinoma, Breast 27830681 D05 D001943 114480 HP:0003002 Novel miRNA genes hypermethylated in breast cancer. epigenetics hsa-mir-132 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-137 Carcinoma, Breast 27830681 D05 D001943 114480 HP:0003002 Novel miRNA genes hypermethylated in breast cancer. epigenetics hsa-mir-137 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-148a Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-152 Carcinoma, Breast 27475839 D05 D001943 114480 HP:0003002 DNA methylation and not H3K4 trimethylation dictates the expression status of miR-152 gene which inhibits migration of breast cancer cells via DNMT1/CDH1 loop. epigenetics hsa-mir-191 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-193a Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-200c Carcinoma, Breast 27717206 D05 D001943 114480 HP:0003002 Epigenetic silencing of miR-200c in breast cancer is associated with aggressiveness and is modulated by ZEB1. epigenetics hsa-mir-203 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-212 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-34b Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-375 Carcinoma, Breast 24571711 D05 D001943 114480 HP:0003002 Epigenetic silencing of miR-375 causes the upregulation of IGF1R,which at least partially underlies trastuzumab resistance of breast cancer cells.Our study has implications for miR-375 as a potential target in combination with trastuzumab for treating HER2-positive breast cancers. epigenetics hsa-mir-375 Carcinoma, Breast 27466996 D05 D001943 114480 HP:0003002 MiR-375 is downregulated in MCF-7/ADM and MCF-7/PTX cells, and its downregulation is a result of promoter methylation. epigenetics hsa-mir-375 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-mir-9 Carcinoma, Breast 27998789 D05 D001943 114480 HP:0003002 DNA methylation contributes to deregulation of 12 cancer-associated microRNAs and breast cancer progression. epigenetics hsa-let-7b Carcinoma, Colon 27525719 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 G9a binds with and stabilizes RelB, thereby recruiting DNA methyltransferase 3 on the Let-7b promoter and repressing its expression. epigenetics hsa-mir-155 Carcinoma, Colon 25502084 gastrointestinal system disease DOID:1520 D01.0 C028885 HP:0003003 miR-200c/141 was downregulated by CpG island methylation and TGF-β signaling, which decreased ZEB1/2 expression and increased E-cadherin expression to inhibit migration and invasion of gastric cancer cells and provides powerful evidence for the application of decitabine in gastric cancer treatment. epigenetics hsa-mir-203 Carcinoma, Endometrial 24530564 reproductive system disease DOID:2871 D07.0 D016889 608089 HP:0012114 Hypermethylation of miR-203 is a frequent event in endometrial carcinomas and is strongly associated with microsatellite instability and MLH1 methylation status. Thus, miR-203 methylation level might represent a marker for patients with endometrioid and clear endometrial sub-cancers. epigenetics hsa-mir-200 Carcinoma, Endometrioid Endometrial 28088687 C54.1 D018269 Whole-Genome DNA Methylation Profiling Identifies Epigenetic Signatures of Uterine Carcinosarcoma. epigenetics hsa-mir-218 Carcinoma, Esophageal 26610476 disease of cellular proliferation DOID:1107 C15.9 D004938 133239 HP:0011459 In conclusion, our results support that aberrant CpG hypermethylation at least partly accounts for miR-218 silencing in ESCC, which impairs its tumor-suppressive function. epigenetics hsa-mir-490 Carcinoma, Gastric 25503559 disease of cellular proliferation DOID:5517 C16.9 D013274 HP:0012126 hypermethylation-mediated silencing of miR-490-3p reactivates SMARCD1 to confer malignant phenotypes, mechanistically linking H. pylori, chromatin remodeling, and gastric carcinogenesis. epigenetics hsa-let-7c Carcinoma, Hepatocellular 22370893 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Enhancer of zeste homolog 2 (EZH2) epigenetically silences multiple tumor suppressor miRNAs (miR-139-5p, miR-125b, miR-101, let-7c, and miR-200b) to promote liver cancer metastasis. epigenetics hsa-mir-101-1 Carcinoma, Hepatocellular 22370893 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Enhancer of zeste homolog 2 (EZH2) epigenetically silences multiple tumor suppressor miRNAs (miR-139-5p, miR-125b, miR-101, let-7c, and miR-200b) to promote liver cancer metastasis. epigenetics hsa-mir-106b Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-122 Carcinoma, Hepatocellular 24085423 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The expression of miRNA-122 is regulated by DNA methylation and correlated with apoptosis of liver cancer cells. Methylation regulation of miRNA-122 expression might be involved in the development of hepatocellular carcinoma. epigenetics hsa-mir-124-1 Carcinoma, Hepatocellular 19843643 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-124:miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma. epigenetics hsa-mir-124-2 Carcinoma, Hepatocellular 19843643 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-124:miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma. epigenetics hsa-mir-124-3 Carcinoma, Hepatocellular 19843643 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-124:miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma. epigenetics hsa-mir-125b-1 Carcinoma, Hepatocellular 22370893 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Enhancer of zeste homolog 2 (EZH2) epigenetically silences multiple tumor suppressor miRNAs (miR-139-5p, miR-125b, miR-101, let-7c, and miR-200b) to promote liver cancer metastasis. epigenetics hsa-mir-125b-2 Carcinoma, Hepatocellular 22370893 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Enhancer of zeste homolog 2 (EZH2) epigenetically silences multiple tumor suppressor miRNAs (miR-139-5p, miR-125b, miR-101, let-7c, and miR-200b) to promote liver cancer metastasis. epigenetics hsa-mir-126 Carcinoma, Hepatocellular 27774652 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 METTL14 suppresses the metastatic potential of hepatocellular carcinoma by modulating N6 -methyladenosine-dependent primary MicroRNA processing. epigenetics hsa-mir-129-1 Carcinoma, Hepatocellular 23580407 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Frequent DNA methylation of MiR-129-2 and its potential clinical implication in hepatocellular carcinoma epigenetics hsa-mir-129-2 Carcinoma, Hepatocellular 23402613 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Methylation-mediated repression of microRNA 129-2 enhances oncogenic SOX4 expression in HCC epigenetics hsa-mir-129-2 Carcinoma, Hepatocellular 23580407 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Frequent DNA methylation of MiR-129-2 and its potential clinical implication in hepatocellular carcinoma epigenetics hsa-mir-139 Carcinoma, Hepatocellular 22370893 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Enhancer of zeste homolog 2 (EZH2) epigenetically silences multiple tumor suppressor miRNAs (miR-139-5p, miR-125b, miR-101, let-7c, and miR-200b) to promote liver cancer metastasis. epigenetics hsa-mir-142 Carcinoma, Hepatocellular 28963738 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Loss-of-function of miR-142 by hypermethylation promotes TGF-β-mediated tumour growth and metastasis in hepatocellular carcinoma. epigenetics hsa-mir-148a Carcinoma, Hepatocellular 24714841 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 MicroRNA-148a is silenced by hypermethylation and interacts with DNA methyltransferase 1 in hepatocellular carcinogenesis. epigenetics hsa-mir-148a Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-152 Carcinoma, Hepatocellular 20578129 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 microRNA-152:a tumor-suppressive role of miR-152 in the epigenetic aberration of HBV-related HCC epigenetics hsa-mir-181a-2 Carcinoma, Hepatocellular 21464043 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 HBx promotes stemness by activating {beta}-catenin and epigenetic up-regulation of miR-181, both of which target EpCAM. epigenetics hsa-mir-181b-1 Carcinoma, Hepatocellular 21464043 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 HBx promotes stemness by activating {beta}-catenin and epigenetic up-regulation of miR-181, both of which target EpCAM. epigenetics hsa-mir-181b-2 Carcinoma, Hepatocellular 21464043 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 HBx promotes stemness by activating {beta}-catenin and epigenetic up-regulation of miR-181, both of which target EpCAM. epigenetics hsa-mir-181c Carcinoma, Hepatocellular 21464043 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 HBx promotes stemness by activating {beta}-catenin and epigenetic up-regulation of miR-181, both of which target EpCAM. epigenetics hsa-mir-181d Carcinoma, Hepatocellular 21464043 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 HBx promotes stemness by activating {beta}-catenin and epigenetic up-regulation of miR-181, both of which target EpCAM. epigenetics hsa-mir-183 Carcinoma, Hepatocellular 28321157 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 hsa-mir-183 is frequently methylated and related to poor survival in human hepatocellular carcinoma. epigenetics hsa-mir-191 Carcinoma, Hepatocellular 21969817 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Hypomethylation of the hsa-miR-191 Locus Causes High Expression of hsa-miR-191 and Promotes the Epithelial-to-Mesenchymal Transition in Hepatocellular Carcinoma. epigenetics hsa-mir-193a Carcinoma, Hepatocellular 22117060 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation regulated miR-193a-3p dictates resistance of hepatocellular carcinoma to 5-fluorouracil via SRSF2. epigenetics hsa-mir-195 Carcinoma, Hepatocellular 17188425 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miRNA-195 expression is decreased in HCC compared to nontumor liver [59], and is also deleted in lung cancer [65], suggesting it is tumor related. miRNA-195 alters the expression of methyl-CpG binding protein 2 (which alters DNA methylation), the SKI oncogene, and a Bcl-2 like protein [59], suggesting miRNA-195 may act as a tumor suppressor in HCC. epigenetics hsa-mir-195 Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-196a-2 Carcinoma, Hepatocellular 21692953 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The CC genotype of the miR-196a-2 rs11614913 polymorphism is associated with increased risk of HCC development in this Turkish population. epigenetics hsa-mir-200a Carcinoma, Hepatocellular 21837748 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 The histone deacetylase 4/Sp1/miR-200a regulatory network contributes to aberrant histone acetylation in hepatocellular carcinoma. epigenetics hsa-mir-200a Carcinoma, Hepatocellular 23222811 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma epigenetics hsa-mir-200b Carcinoma, Hepatocellular 22370893 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Enhancer of zeste homolog 2 (EZH2) epigenetically silences multiple tumor suppressor miRNAs (miR-139-5p, miR-125b, miR-101, let-7c, and miR-200b) to promote liver cancer metastasis. epigenetics hsa-mir-200b Carcinoma, Hepatocellular 23222811 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma epigenetics hsa-mir-200c Carcinoma, Hepatocellular 23222811 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma epigenetics hsa-mir-203 Carcinoma, Hepatocellular 19843643 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-203:miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma. epigenetics hsa-mir-223 Carcinoma, Hepatocellular 24333181 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Downregulation of miR-223 in HCC is associated with the epigenetic regulation by highly expressed sulfatide and involved in tumor metastasis. epigenetics hsa-mir-224 Carcinoma, Hepatocellular 22459148 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 MicroRNA-224 is up-regulated in hepatocellular carcinoma through epigenetic mechanisms. epigenetics hsa-mir-23a Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-25 Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-27a Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-29a Carcinoma, Hepatocellular 23789939 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-29a could regulate TGF-β-induced EMT by affecting DNA methylation via the suppression of DNMT. epigenetics hsa-mir-302 Carcinoma, Hepatocellular 24740829 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 miR-302-mediated iPSC technology reprogrammed HCC cells and improved drug sensitivity through AOF2 down-regulation, which caused H3K4 methylation and c-Myc repression. epigenetics hsa-mir-335 Carcinoma, Hepatocellular 23229728 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Epigenetic silencing of miR-335 and its host gene MEST in hepatocellular carcinoma epigenetics hsa-mir-34b Carcinoma, Hepatocellular 24704024 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Methylation-associated silencing of microRNA-34b in hepatocellular carcinoma cancer. epigenetics hsa-mir-375 Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-378 Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-429 Carcinoma, Hepatocellular 24572141 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 Epigenetic modification of miR-429 can manipulate liver T-ICs by targeting the RBBP4/E2F1/OCT4 axis. This miRNA might be targeted to inactivate T-ICs, thus providing a novel strategy for HCC prevention and treatment. epigenetics hsa-mir-497 Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-519d Carcinoma, Hepatocellular 22262409 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 In hepatocellular carcinoma miR-519d is upregulated by p53 and DNA hypomethylation and targets CDKN1A/p21, PTEN, AKT3 and TIMP2. epigenetics hsa-mir-615 Carcinoma, Hepatocellular 27487123 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 In conclusion, our findings characterize miR-615-5p as an important epigenetically silenced miRNA involved in the Rab-Ras pathway in hepatocellular carcinoma and expand our understanding of the molecular mechanism underlying hepatocarcinogenesis and metastasis. epigenetics hsa-mir-93 Carcinoma, Hepatocellular 25424171 disease of cellular proliferation DOID:684 C22.0 D006528 114550 HP:0001402 DNA methylation plays an important and complex role in the regulation of miRNA expression in HCC, which may provide insights into the pathogenesis of HCC and thus may be used for diagnosis and intervention. epigenetics hsa-mir-137 Carcinoma, Lung, Non-Small-Cell 28223039 C34.90 D002289 HP:0030358 Oncogene LSD1 is epigenetically suppressed by miR-137 overexpression in human non-small cell lung cancer. epigenetics hsa-mir-124-2 Carcinoma, Lung, Non-Small-Cell 21917081 C34.90 D002289 HP:0030358 The methylation of mir-9-3, -124-2, and -124-3 was individually associated with an advanced T factor independently of age, sex, and smoking habit. epigenetics hsa-mir-124-3 Carcinoma, Lung, Non-Small-Cell 21917081 C34.90 D002289 HP:0030358 The methylation of mir-9-3, -124-2, and -124-3 was individually associated with an advanced T factor independently of age, sex, and smoking habit. epigenetics hsa-mir-126 Carcinoma, Lung, Non-Small-Cell 21702040 C34.90 D002289 HP:0030358 mir-34b and mir-126 were silenced by DNA methylation. epigenetics hsa-mir-139 Carcinoma, Lung, Non-Small-Cell 26256448 C34.90 D002289 HP:0030358 Histone methylation-mediated silencing of miR-139 enhances invasion of non-small-cell lung cancer. epigenetics hsa-mir-15a Carcinoma, Lung, Non-Small-Cell 23867991 C34.90 D002289 HP:0030358 Histone deacetylases inhibitor trichostatin A increases the expression of Dleu2/miR-15a/16-1 via HDAC3 in non-small cell lung cancer. epigenetics hsa-mir-16-1 Carcinoma, Lung, Non-Small-Cell 23867991 C34.90 D002289 HP:0030358 Histone deacetylases inhibitor trichostatin A increases the expression of Dleu2/miR-15a/16-1 via HDAC3 in non-small cell lung cancer. epigenetics hsa-mir-193a Carcinoma, Lung, Non-Small-Cell 22282464 C34.90 D002289 HP:0030358 Genome-Wide miRNA Expression Profiling Identifies miR-9-3 and miR-193a as Targets for DNA Methylation in Non-Small Cell Lung Cancers. epigenetics hsa-mir-199a-1 Carcinoma, Lung, Non-Small-Cell 21317930 C34.90 D002289 HP:0030358 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-199a-2 Carcinoma, Lung, Non-Small-Cell 21317930 C34.90 D002289 HP:0030358 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-199b Carcinoma, Lung, Non-Small-Cell 21317930 C34.90 D002289 HP:0030358 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-212 Carcinoma, Lung, Non-Small-Cell 22110741 C34.90 D002289 HP:0030358 We identified histone modifications rather than DNA hypermethylation as epigenetic events that regulate miR-212 levels in NSCLC. Moreover, we found that miR-212 silencing in vivo is closely associated with the severity of the disease. epigenetics hsa-mir-29 Carcinoma, Lung, Non-Small-Cell 23939044 C34.90 D002289 HP:0030358 Suppression of Wnt signaling by the miR-29 family is mediated by demethylation of WIF-1 in non-small-cell lung cancer. epigenetics hsa-mir-34a Carcinoma, Lung, Non-Small-Cell 21317930 C34.90 D002289 HP:0030358 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-34b Carcinoma, Lung, Non-Small-Cell 21383543 C34.90 D002289 HP:0030358 DNA hypermethylation of microRNA-34b/c has prognostic value for stage Ⅰ non-small cell lung cancer. epigenetics hsa-mir-34b Carcinoma, Lung, Non-Small-Cell 21702040 C34.90 D002289 HP:0030358 mir-34b and mir-126 were silenced by DNA methylation. epigenetics hsa-mir-34c Carcinoma, Lung, Non-Small-Cell 21383543 C34.90 D002289 HP:0030358 DNA hypermethylation of microRNA-34b/c has prognostic value for stage Ⅰ non-small cell lung cancer. epigenetics hsa-mir-9-3 Carcinoma, Lung, Non-Small-Cell 21917081 C34.90 D002289 HP:0030358 The methylation of mir-9-3, -124-2, and -124-3 was individually associated with an advanced T factor independently of age, sex, and smoking habit. epigenetics hsa-mir-9-3 Carcinoma, Lung, Non-Small-Cell 22282464 C34.90 D002289 HP:0030358 Genome-Wide miRNA Expression Profiling Identifies miR-9-3 and miR-193a as Targets for DNA Methylation in Non-Small Cell Lung Cancers. epigenetics hsa-mir-34b Carcinoma, Lung, Small-Cell 22047961 C34.90 D055752 182280 HP:0030357 Frequent methylation and oncogenic role of microRNA-34b/c in small-cell lung cancer. epigenetics hsa-mir-34c Carcinoma, Lung, Small-Cell 22047961 C34.90 D055752 182280 HP:0030357 Frequent methylation and oncogenic role of microRNA-34b/c in small-cell lung cancer. epigenetics hsa-mir-148a Carcinoma, Nasopharyngeal 25277193 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Silencing of miRNA-148a by hypermethylation activates the integrin-mediated signaling pathway in nasopharyngeal carcinoma. epigenetics hsa-mir-24 Carcinoma, Nasopharyngeal 25319395 disease of cellular proliferation DOID:9261 C11 C538339 607107 HP:0100630 Involvement of microRNA-24 and DNA methylation in resistance of nasopharyngeal carcinoma to ionizing radiation. epigenetics hsa-mir-127 Carcinoma, Oral 22132151 gastrointestinal system disease DOID:0050610 MiR-375 is repressed and miR-127 activated in OSCC, and we confirm previous reports of miR-137 hypermethylation in oral cancer. The miR-200 s/miR-205 were epigenetically activated in tumors vs normal tissues, but repressed in the absence of DNA hypermethylation specifically in CD44(high) oral CSCs. Aberrant miR-375 and miR-200a expression and miR-200c-141 methylation could be detected in and distinguish OSCC patient oral rinse and saliva from healthy volunteers. epigenetics hsa-mir-137 Carcinoma, Oral 22132151 gastrointestinal system disease DOID:0050610 MiR-375 is repressed and miR-127 activated in OSCC, and we confirm previous reports of miR-137 hypermethylation in oral cancer. The miR-200 s/miR-205 were epigenetically activated in tumors vs normal tissues, but repressed in the absence of DNA hypermethylation specifically in CD44(high) oral CSCs. Aberrant miR-375 and miR-200a expression and miR-200c-141 methylation could be detected in and distinguish OSCC patient oral rinse and saliva from healthy volunteers. epigenetics hsa-mir-141 Carcinoma, Oral 22132151 gastrointestinal system disease DOID:0050610 MiR-375 is repressed and miR-127 activated in OSCC, and we confirm previous reports of miR-137 hypermethylation in oral cancer. The miR-200 s/miR-205 were epigenetically activated in tumors vs normal tissues, but repressed in the absence of DNA hypermethylation specifically in CD44(high) oral CSCs. Aberrant miR-375 and miR-200a expression and miR-200c-141 methylation could be detected in and distinguish OSCC patient oral rinse and saliva from healthy volunteers. epigenetics hsa-mir-200a Carcinoma, Oral 22132151 gastrointestinal system disease DOID:0050610 MiR-375 is repressed and miR-127 activated in OSCC, and we confirm previous reports of miR-137 hypermethylation in oral cancer. The miR-200 s/miR-205 were epigenetically activated in tumors vs normal tissues, but repressed in the absence of DNA hypermethylation specifically in CD44(high) oral CSCs. Aberrant miR-375 and miR-200a expression and miR-200c-141 methylation could be detected in and distinguish OSCC patient oral rinse and saliva from healthy volunteers. epigenetics hsa-mir-200c Carcinoma, Oral 22132151 gastrointestinal system disease DOID:0050610 MiR-375 is repressed and miR-127 activated in OSCC, and we confirm previous reports of miR-137 hypermethylation in oral cancer. The miR-200 s/miR-205 were epigenetically activated in tumors vs normal tissues, but repressed in the absence of DNA hypermethylation specifically in CD44(high) oral CSCs. Aberrant miR-375 and miR-200a expression and miR-200c-141 methylation could be detected in and distinguish OSCC patient oral rinse and saliva from healthy volunteers. epigenetics hsa-mir-375 Carcinoma, Oral 22132151 gastrointestinal system disease DOID:0050610 MiR-375 is repressed and miR-127 activated in OSCC, and we confirm previous reports of miR-137 hypermethylation in oral cancer. The miR-200 s/miR-205 were epigenetically activated in tumors vs normal tissues, but repressed in the absence of DNA hypermethylation specifically in CD44(high) oral CSCs. Aberrant miR-375 and miR-200a expression and miR-200c-141 methylation could be detected in and distinguish OSCC patient oral rinse and saliva from healthy volunteers. epigenetics hsa-mir-375 Carcinoma, Ovarian 29631007 endocrine system disease DOID:4001 C56.9 C538090 167000 HP:0025318 Novel miRNA genes deregulated by aberrant methylation in ovarian carcinoma are involved in metastasis epigenetics hsa-mir-124-1 Carcinoma, Renal Cell 23321515 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Hsa-mir-124-3 CpG island methylation is associated with advanced tumours and disease recurrence of patients with clear cell renal cell carcinoma epigenetics hsa-mir-124-2 Carcinoma, Renal Cell 23321515 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Hsa-mir-124-3 CpG island methylation is associated with advanced tumours and disease recurrence of patients with clear cell renal cell carcinoma epigenetics hsa-mir-124-3 Carcinoma, Renal Cell 23321515 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Hsa-mir-124-3 CpG island methylation is associated with advanced tumours and disease recurrence of patients with clear cell renal cell carcinoma epigenetics hsa-mir-124a-2 Carcinoma, Renal Cell 23755536 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The frequency of methylation of six genes (miR-124a-2, -124a-3, -9-1, -9-3, -34b/c and -129-2) was significantly higher in tumor samples than in samples of histologically normal tissue epigenetics hsa-mir-124a-3 Carcinoma, Renal Cell 23755536 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The frequency of methylation of six genes (miR-124a-2, -124a-3, -9-1, -9-3, -34b/c and -129-2) was significantly higher in tumor samples than in samples of histologically normal tissue epigenetics hsa-mir-129-2 Carcinoma, Renal Cell 23755536 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The frequency of methylation of six genes (miR-124a-2, -124a-3, -9-1, -9-3, -34b/c and -129-2) was significantly higher in tumor samples than in samples of histologically normal tissue epigenetics hsa-mir-34a Carcinoma, Renal Cell 21225432 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Carcinoma, Renal Cell 21225432 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Carcinoma, Renal Cell 23755536 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The frequency of methylation of six genes (miR-124a-2, -124a-3, -9-1, -9-3, -34b/c and -129-2) was significantly higher in tumor samples than in samples of histologically normal tissue epigenetics hsa-mir-34c Carcinoma, Renal Cell 21225432 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Carcinoma, Renal Cell 23755536 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The frequency of methylation of six genes (miR-124a-2, -124a-3, -9-1, -9-3, -34b/c and -129-2) was significantly higher in tumor samples than in samples of histologically normal tissue epigenetics hsa-mir-9-1 Carcinoma, Renal Cell 23755536 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The frequency of methylation of six genes (miR-124a-2, -124a-3, -9-1, -9-3, -34b/c and -129-2) was significantly higher in tumor samples than in samples of histologically normal tissue epigenetics hsa-mir-9-3 Carcinoma, Renal Cell 23755536 disease of cellular proliferation DOID:4450 D002292 144700 HP:0005584 The frequency of methylation of six genes (miR-124a-2, -124a-3, -9-1, -9-3, -34b/c and -129-2) was significantly higher in tumor samples than in samples of histologically normal tissue epigenetics hsa-mir-129 Carcinoma, Urothelial 28081549 disease of cellular proliferation DOID:4006 HP:0030409 MicroRNA promoter methylation: a new tool for accurate detection of urothelial carcinoma. epigenetics hsa-mir-663a Carcinoma, Urothelial 28081549 disease of cellular proliferation DOID:4006 HP:0030409 MicroRNA promoter methylation: a new tool for accurate detection of urothelial carcinoma. epigenetics hsa-mir-1 Cardiomegaly 18539123 I51.7 D006332 HP:0001640 Microinjecting fragments of either the coding region or the related microRNA miR-1 led to high levels of expression of homologous RNA, resulting in an epigenetic defect, cardiac hypertrophy, whose efficient hereditary transmission correlated with the presence of miR-1 in the sperm nucleus. epigenetics hsa-mir-133a Cardiomegaly 26830171 I51.7 D006332 HP:0001640 Phe exposure led to methylation of CpG sites within the miR-133a locus and reduced miR-133a expression in H9C2 cells epigenetics hsa-let-7c Cardiomyopathy 24365598 cardiovascular system disease DOID:0050700 I42 D009202 Cardiomyogenesis is controlled by the miR-99a/let-7c cluster and epigenetic modifications. epigenetics hsa-mir-99a Cardiomyopathy 24365598 cardiovascular system disease DOID:0050700 I42 D009202 Cardiomyogenesis is controlled by the miR-99a/let-7c cluster and epigenetic modifications. epigenetics hsa-mir-210 Cardiovascular Diseases [unspecific] 26254226 D002318 Oxidized low-density lipoprotein is a common risk factor for cardiovascular diseases and gastroenterological cancers via epigenomical regulation of microRNA-210. epigenetics hsa-mir-29b Cardiovascular Diseases [unspecific] 22226905 D002318 This article is part of a Special Issue entitled OxLDL causes both epigenetic modification and signaling regulation on the microRNA-29b gene: Novel mechanisms for cardiovascular diseases. epigenetics hsa-mir-124 Cervical Neoplasms 27765948 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 Suppression of iASPP-dependent aggressiveness in cervical cancer through reversal of methylation silencing of microRNA-124. epigenetics hsa-mir-200b Cervical Neoplasms 27272214 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 Long noncoding RNA PVT1 promotes cervical cancer progression through epigenetically silencing miR-200b epigenetics hsa-mir-200b Cervical Neoplasms 29077234 disease of cellular proliferation DOID:4362 C53.9 D002583 603956 HP:0030159 DNA methylation regulated microRNAs in human cervical cancer. epigenetics hsa-mir-124-1 Cholangiocarcinoma 22819820 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 Epigenetic regulation of miR-124 by Hepatitis C Virus core protein promotes migration and invasion of intrahepatic cholangiocarcinoma cells by targeting SMYD3. epigenetics hsa-mir-124-2 Cholangiocarcinoma 22819820 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 Epigenetic regulation of miR-124 by Hepatitis C Virus core protein promotes migration and invasion of intrahepatic cholangiocarcinoma cells by targeting SMYD3. epigenetics hsa-mir-34a Cholangiocarcinoma 28923203 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 Epigenetic Silencing of miRNA-34a in Human Cholangiocarcinoma via EZH2 and DNA Methylation: Impact on Regulation of Notch Pathway. epigenetics hsa-mir-370 Cholangiocarcinoma 28545228 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 Aberrant DNA Methylation as a Biomarker and a Therapeutic Target of Cholangiocarcinoma. epigenetics hsa-mir-373 Cholangiocarcinoma 21165562 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 Methyl-CpG binding protein MBD2 is implicated in methylation-mediated suppression of miR-373 in hilar Cholangiocarcinoma. epigenetics hsa-mir-429 Cholangiocarcinoma 27593557 disease of cellular proliferation DOID:4947 C22.1 D018281 615619 HP:0030153 Cadherin-6 is a putative tumor suppressor and target of epigenetically dysregulated miR-429 in cholangiocarcinoma. epigenetics hsa-mir-125b Chondrosarcoma 27576314 disease of cellular proliferation DOID:3371 M91-M94 D002813 215300 HP:0006765 Induction of the mesenchymal to epithelial transition by demethylation-activated microRNA-125b is involved in the anti-migration/invasion effects of arsenic trioxide on human chondrosarcoma. epigenetics hsa-mir-145 Chondrosarcoma 25145279 disease of cellular proliferation DOID:3371 M91-M94 D002813 215300 HP:0006765 The epigenetic regulation of SOX9 by miR-145 in human chondrosarcoma. epigenetics hsa-mir-302c Chondrosarcoma 26094604 disease of cellular proliferation DOID:3371 M91-M94 D002813 215300 HP:0006765 Epigenetic regulation of embryonic stem cell marker miR302C in human chondrosarcoma as determinant of antiproliferative activity of proline-rich polypeptide 1. epigenetics hsa-mir-219 Chronic Inflammatory Pain 25031391 methylation-mediated epigenetic modification of spinal miR-219 expression regulates chronic inflammatory pain by targeting CaMKIIγ. epigenetics hsa-mir-199a Chronic Obstructive Pulmonary Disease 24299514 respiratory system disease DOID:3083 J44.9 D029424 606963 HP:0006510 miR-199a-5p is a key regulator of the unfolded protein response in AAT-deficient monocytes, and epigenetic silencing of its expression regulates this process in chronic obstructive pulmonary disease. epigenetics hsa-mir-24 Colon Adenoma 26559563 disease of cellular proliferation DOID:0050912 Butyrate and partial TSA reduced the expression of miR-135a, miR-135b, miR-24 and miR-let-7a (~0.5-fold, 24 h) and miR-24, miR-106b and miR-let-7a (~0.5-0.7-fold, 48 h) in LT97 cells. epigenetics hsa-mir-127 Colon Neoplasms 17355635 D12.6 D003110 HP:0100273 Human miR-127 is embedded in a CpG island and is silenced in several human cancers including bladder, prostate and colon cancer and has been suggested to play a role as a possible tumour suppressor gene. epigenetics hsa-mir-34a Colon Neoplasms 23243217 D12.6 D003110 HP:0100273 Detection of miR-34a Promoter Methylation in Combination with Elevated Expression of c-Met and beta-Catenin Predicts Distant Metastasis of Colon Cancer epigenetics hsa-mir-124a Colorectal Carcinoma 22870149 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The results showed that the methylation of miR-124a and miR-34b/c occured early in colorectal carcinogenesis and certain CRCs may arise from a field defect defined by the epigenetic inactivation of miRs. epigenetics hsa-mir-125a Colorectal Carcinoma 26693202 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Our results suggest that DNA hypermethylation may be involved in the inactivation of miR-125a and miR-125b in CRC, and hypermethylation of miR-125 is a potential biomarker for clinical outcome. epigenetics hsa-mir-125b Colorectal Carcinoma 26693202 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Our results suggest that DNA hypermethylation may be involved in the inactivation of miR-125a and miR-125b in CRC, and hypermethylation of miR-125 is a potential biomarker for clinical outcome. epigenetics hsa-mir-126 Colorectal Carcinoma 23900443 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Epigenetic silencing of miR-126 contributes to tumor invasion and angiogenesis in colorectal cancer. epigenetics hsa-mir-21 Colorectal Carcinoma 26787105 disease of cellular proliferation DOID:0080199 C19 D015179 114500 This study suggests a high frequency of miR-21 overexpression and aberrant promoter methylation in down-regulation of PTEN expression in colorectal carcinoma. Loss of PTEN may be a prognostic factor for patients with CRC. epigenetics hsa-mir-210 Colorectal Carcinoma 28364795 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The significance of DNA methylation profile in metastasis-related genes for the progression of colorectal cancer. epigenetics hsa-mir-34 Colorectal Carcinoma 28364795 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The significance of DNA methylation profile in metastasis-related genes for the progression of colorectal cancer. epigenetics hsa-mir-34a Colorectal Carcinoma 25422210 disease of cellular proliferation DOID:0080199 C19 D015179 114500 miRNA-34a-5p may play a role as a tumor suppressor gene in colorectal cancer, with involvement of DNA methylation. epigenetics hsa-mir-34b Colorectal Carcinoma 18519671 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Our results suggest that miR-34b/c and BTG4 are novel tumor suppressors in CRC and that the miR-34b/c CpG island, which bidirectionally regulates miR-34b/c and BTG4, is a frequent target of epigenetic silencing in CRC. epigenetics hsa-mir-34b Colorectal Carcinoma 22870149 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The results showed that the methylation of miR-124a and miR-34b/c occured early in colorectal carcinogenesis and certain CRCs may arise from a field defect defined by the epigenetic inactivation of miRs. epigenetics hsa-mir-34c Colorectal Carcinoma 26704889 disease of cellular proliferation DOID:0080199 C19 D015179 114500 In conclusion, our results suggested the existence of E2F1-miR-34c-SCF negative feedback loop which was interrupted by the hyper-methylation of miR-34c promoter in CRC cells and increased cell proliferation. epigenetics hsa-mir-34c Colorectal Carcinoma 18519671 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Our results suggest that miR-34b/c and BTG4 are novel tumor suppressors in CRC and that the miR-34b/c CpG island, which bidirectionally regulates miR-34b/c and BTG4, is a frequent target of epigenetic silencing in CRC. epigenetics hsa-mir-34c Colorectal Carcinoma 22870149 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The results showed that the methylation of miR-124a and miR-34b/c occured early in colorectal carcinogenesis and certain CRCs may arise from a field defect defined by the epigenetic inactivation of miRs. epigenetics hsa-mir-484 Colorectal Carcinoma 25727216 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Methylation-induced loss of miR-484 in microsatellite-unstable colorectal cancer promotes both viability and IL-8 production via CD137L. epigenetics hsa-mir-9 Colorectal Carcinoma 28364795 disease of cellular proliferation DOID:0080199 C19 D015179 114500 The significance of DNA methylation profile in metastasis-related genes for the progression of colorectal cancer. epigenetics hsa-mir-1-1 Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-1-1 Colorectal Carcinoma 22766685 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Silencing of miR-1-1 and miR-133a-2 cluster expression by DNA hypermethylation in colorectal cancer. epigenetics hsa-mir-124-1 Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-2 Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-3 Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-133a-1 Colorectal Carcinoma 22766685 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Silencing of miR-1-1 and miR-133a-2 cluster expression by DNA hypermethylation in colorectal cancer. epigenetics hsa-mir-133a-2 Colorectal Carcinoma 22766685 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Silencing of miR-1-1 and miR-133a-2 cluster expression by DNA hypermethylation in colorectal cancer. epigenetics hsa-mir-148a Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-149 Colorectal Carcinoma 22821729 disease of cellular proliferation DOID:0080199 C19 D015179 114500 SP1 mediates the link between methylation of the tumour suppressor miR-149 and outcome in colorectal cancer. epigenetics hsa-mir-149 Colorectal Carcinoma 23115050 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Non-CpG island promoter hypomethylation and miR-149 regulate the expression of SRPX2 in colorectal cancer epigenetics hsa-mir-152 Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-17 Colorectal Carcinoma 22308110 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Histone deacetylase inhibition in colorectal cancer cells reveals competing roles for members of the oncogenic miR-17-92 cluster. epigenetics hsa-mir-18a Colorectal Carcinoma 22308110 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Histone deacetylase inhibition in colorectal cancer cells reveals competing roles for members of the oncogenic miR-17-92 cluster. epigenetics hsa-mir-18b Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-199a-1 Colorectal Carcinoma 21317930 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-199a-2 Colorectal Carcinoma 21317930 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-199b Colorectal Carcinoma 21317930 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-19a Colorectal Carcinoma 22308110 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Histone deacetylase inhibition in colorectal cancer cells reveals competing roles for members of the oncogenic miR-17-92 cluster. epigenetics hsa-mir-19b-1 Colorectal Carcinoma 22308110 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Histone deacetylase inhibition in colorectal cancer cells reveals competing roles for members of the oncogenic miR-17-92 cluster. epigenetics hsa-mir-200a Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-208a Colorectal Carcinoma 21327300 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-20a Colorectal Carcinoma 22308110 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Histone deacetylase inhibition in colorectal cancer cells reveals competing roles for members of the oncogenic miR-17-92 cluster. epigenetics hsa-mir-345 Colorectal Carcinoma 21665895 disease of cellular proliferation DOID:0080199 C19 D015179 114500 MicroRNA 345, a methylation-sensitive microRNA is involved in cell proliferation and invasion in human colorectal cancer. epigenetics hsa-mir-34a Colorectal Carcinoma 21225432 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34a Colorectal Carcinoma 21317930 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Axl receptor expression can be regulated by miR-34a and miR-199a/b, which are suppressed by promoter methylation in solid cancer cells epigenetics hsa-mir-34b Colorectal Carcinoma 21225432 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Colorectal Carcinoma 21610744 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Epigenetically silenced miR-34b/c as a novel faecal-based screening marker for colorectal cancer. epigenetics hsa-mir-34c Colorectal Carcinoma 21225432 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Colorectal Carcinoma 21610744 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Epigenetically silenced miR-34b/c as a novel faecal-based screening marker for colorectal cancer. epigenetics hsa-mir-373 Colorectal Carcinoma 21785829 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Epigenetic silencing of microRNA-373 plays an important role in regulating cell proliferation in colon cancer. epigenetics hsa-mir-92a-1 Colorectal Carcinoma 22308110 disease of cellular proliferation DOID:0080199 C19 D015179 114500 Histone deacetylase inhibition in colorectal cancer cells reveals competing roles for members of the oncogenic miR-17-92 cluster. epigenetics hsa-mir-375 Diabetes Mellitus, Type 2 24366165 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Expression and DNA methylation status of microRNA-375 in patients with type 2 diabetes mellitus. epigenetics hsa-mir-375 Diabetes Mellitus, Type 2 24741571 disease of metabolism DOID:9352 E11 D003924 125853 HP:0005978 Ethnic differences in microRNA-375 expression level and DNA methylation status in type 2 diabetes of Han and Kazak populations. epigenetics hsa-mir-34b Early-Stage Lung Adenocarcinoma 24130071 C34.90 C538231 211980 Epigenetic inactivation of microRNA-34b/c predicts poor disease-free survival in early-stage lung adenocarcinoma. epigenetics hsa-mir-34c Early-Stage Lung Adenocarcinoma 24130071 C34.90 C538231 211980 Epigenetic inactivation of microRNA-34b/c predicts poor disease-free survival in early-stage lung adenocarcinoma. epigenetics hsa-mir-1-1 Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-1 Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-2 Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-3 Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-148a Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-152 Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-152 Endometrial Neoplasms 21868754 reproductive system disease DOID:1380 C54.1 D016889 608089 miR-152 is a tumor suppressor microRNA that is silenced by DNA hypermethylation in endometrial cancer. epigenetics hsa-mir-18b Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-200a Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-208a Endometrial Neoplasms 21327300 reproductive system disease DOID:1380 C54.1 D016889 608089 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-675 Eosinophilic Esophagitis 22391115 gastrointestinal system disease DOID:13922 K20.0 D057765 610247 EoE remission induced a single miRNA (miR-675) likely to be involved in DNA methylation. epigenetics hsa-mir-129-2 Esophageal Neoplasms 21547903 C15.9 D004938 133239 HP:0100751 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-141 Esophageal Neoplasms 22921431 C15.9 D004938 133239 HP:0100751 Inhibition of SOX17 by MicroRNA-141 and Methylation Activates the WNT Signaling Pathway in Esophageal Cancer. epigenetics hsa-mir-34a Esophageal Neoplasms 21547903 C15.9 D004938 133239 HP:0100751 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-34b Esophageal Neoplasms 21547903 C15.9 D004938 133239 HP:0100751 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-34c Esophageal Neoplasms 21547903 C15.9 D004938 133239 HP:0100751 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-375 Esophageal Neoplasms 21533613 C15.9 D004938 133239 HP:0100751 Epigenetic Silencing of MicroRNA-375 Regulates PDK1 Expression in Esophageal Cancer epigenetics hsa-mir-22 Ewing Sarcoma 24362521 musculoskeletal system disease DOID:3369 D012512 612219 HP:0012254 The histone demethylase KDM3A is a microRNA-22-regulated tumor promoter in Ewing Sarcoma. epigenetics hsa-mir-10b Gastric Neoplasms 24481854 disease of cellular proliferation DOID:10534 C16 D013274 137215 Taken together, these findings suggest that miR-10b may function as a novel tumor suppressor and is partially silenced by DNA hypermethylation in GC. epigenetics hsa-mir-10b Gastric Neoplasms 21562367 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-10b methylation may be a useful molecular biomarker for assessing the risk of gastric cancer development, and modulation of miR-10b may represent a therapeutic approach for treating gastric cancer. epigenetics hsa-mir-124-1 Gastric Neoplasms 21365509 disease of cellular proliferation DOID:10534 C16 D013274 137215 Significant associations were found between hypermethylation of hsa-miR-124a and tumor size, differentiation, lymphatic metastasis, and invasion depth(P<0.01). epigenetics hsa-mir-124-1 Gastric Neoplasms 21914401 disease of cellular proliferation DOID:10534 C16 D013274 137215 The hypermethylation of miRNA-34b/c and miRNA-124a gene promoters may play a crucial role in the occurrence and development of gastric carcinoma. epigenetics hsa-mir-124-2 Gastric Neoplasms 21365509 disease of cellular proliferation DOID:10534 C16 D013274 137215 Significant associations were found between hypermethylation of hsa-miR-124a and tumor size, differentiation, lymphatic metastasis, and invasion depth(P<0.01). epigenetics hsa-mir-124-3 Gastric Neoplasms 21365509 disease of cellular proliferation DOID:10534 C16 D013274 137215 Significant associations were found between hypermethylation of hsa-miR-124a and tumor size, differentiation, lymphatic metastasis, and invasion depth(P<0.01). epigenetics hsa-mir-129 Gastric Neoplasms 25344911 disease of cellular proliferation DOID:10534 C16 D013274 137215 Methylation of miR-129-5p CpG island modulates multi-drug resistance in gastric cancer by targeting ABC transporters. epigenetics hsa-mir-129-2 Gastric Neoplasms 21213213 disease of cellular proliferation DOID:10534 C16 D013274 137215 upstream CpG-rich regions of mir-34b and mir-129-2 are frequently methylated in gastric cancer tissues compared with adjacent normal tissues, and their methylation status correlated inversely with their expression patterns. epigenetics hsa-mir-129-2 Gastric Neoplasms 21960261 disease of cellular proliferation DOID:10534 C16 D013274 137215 The methylation-silenced expression of the miRNA could be reactivated in gastric cancer cells by treatment with demethylating drugs in a time-dependent manner.Analysis of the methylation status of these miRNAs showed that the upstream CpG-rich regions of mir-34b and mir-129-2 are frequently methylated in gastric cancer tissues compared to adjacent normal tissues, and their methylation status correlated inversely with their expression patterns. The expression of miR-34b and miR-129-3p was downregulated by DNA hypermethylation in primary gastric cancers, and the low expression was associated with poor clinicopathological features. epigenetics hsa-mir-137 Gastric Neoplasms 22703336 disease of cellular proliferation DOID:10534 C16 D013274 137215 Methylation frequency of 5 miR CpG islands (miR-9-1, miR-9-3, miR-137, miR-34b, and miR-210) gradually increased while the proportion of methylated miR-200b gradually decreased during gastric carcinogenesis epigenetics hsa-mir-139 Gastric Neoplasms 21925125 disease of cellular proliferation DOID:10534 C16 D013274 137215 HER2 Interacts with CD44 to Upregulate CXCR4 via Epigenetic Silencing of microRNA-139 in Gastric Cancer Cells. epigenetics hsa-mir-141 Gastric Neoplasms 25502084 disease of cellular proliferation DOID:10534 C16 D013274 137215 sion of miR-200c/141 induced by TGF-β in SGC-7901 cells. Our study revealed that miR-200c/141 was downregulated by CpG island methylation and TGF-β signaling, which decreased ZEB1/2 expression and increased E-cadherin expression to inhibit migration and invasion of gastric cancer cells and provides powerful evidence for the application of decitabine in gastric cancer treatment. epigenetics hsa-mir-148a Gastric Neoplasms 22167392 disease of cellular proliferation DOID:10534 C16 D013274 137215 MicroRNA-148a is silenced by hypermethylation and interacts with DNA methyltransferase 1 in gastric cancer. epigenetics hsa-mir-181c Gastric Neoplasms 20080834 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-181c:Involvement of epigenetically silenced microRNA-181c in gastric carcinogenesis. epigenetics hsa-mir-195 Gastric Neoplasms 23333942 disease of cellular proliferation DOID:10534 C16 D013274 137215 MicroRNA-195 and microRNA-378 mediate tumor growth suppression by epigenetical regulation in gastric cancer epigenetics hsa-mir-200 Gastric Neoplasms 25502084 disease of cellular proliferation DOID:10534 C16 D013274 137215 sion of miR-200c/141 induced by TGF-β in SGC-7901 cells. Our study revealed that miR-200c/141 was downregulated by CpG island methylation and TGF-β signaling, which decreased ZEB1/2 expression and increased E-cadherin expression to inhibit migration and invasion of gastric cancer cells and provides powerful evidence for the application of decitabine in gastric cancer treatment. epigenetics hsa-mir-210 Gastric Neoplasms 22703336 disease of cellular proliferation DOID:10534 C16 D013274 137215 Methylation frequency of 5 miR CpG islands (miR-9-1, miR-9-3, miR-137, miR-34b, and miR-210) gradually increased while the proportion of methylated miR-200b gradually decreased during gastric carcinogenesis epigenetics hsa-mir-212 Gastric Neoplasms 20020497 disease of cellular proliferation DOID:10534 C16 D013274 137215 miR-212:miR-212 is downregulated and suppresses methyl-CpG-binding protein MeCP2 in human gastric cancer epigenetics hsa-mir-29b Gastric Neoplasms 25874772 disease of cellular proliferation DOID:10534 C16 D013274 137215 Deregulation between miR-29b/c and DNMT3A is associated with epigenetic silencing of the CDH1 gene, affecting cell migration and invasion in gastric cancer. epigenetics hsa-mir-29c Gastric Neoplasms 25874772 disease of cellular proliferation DOID:10534 C16 D013274 137215 Deregulation between miR-29b/c and DNMT3A is associated with epigenetic silencing of the CDH1 gene, affecting cell migration and invasion in gastric cancer. epigenetics hsa-mir-30b Gastric Neoplasms 24913034 disease of cellular proliferation DOID:10534 C16 D013274 137215 Decreased miR-30b-5p expression by DNMT1 methylation regulation involved in gastric cancer metastasis. epigenetics hsa-mir-34a Gastric Neoplasms 25860861 disease of cellular proliferation DOID:10534 C16 D013274 137215 Sirt7 promotes gastric cancer growth and inhibits apoptosis by epigenetically inhibiting miR-34a. epigenetics hsa-mir-34b Gastric Neoplasms 23942619 disease of cellular proliferation DOID:10534 C16 D013274 137215 Our results suggest that methylation of miR-34b/c in the mucosa of the noncancerous gastric body may be a useful biomarker for predicting the risk of metachronous GC. epigenetics hsa-mir-34b Gastric Neoplasms 21213213 disease of cellular proliferation DOID:10534 C16 D013274 137215 upstream CpG-rich regions of mir-34b and mir-129-2 are frequently methylated in gastric cancer tissues compared with adjacent normal tissues, and their methylation status correlated inversely with their expression patterns. epigenetics hsa-mir-34b Gastric Neoplasms 21914401 disease of cellular proliferation DOID:10534 C16 D013274 137215 The hypermethylation of miRNA-34b/c and miRNA-124a gene promoters may play a crucial role in the occurrence and development of gastric carcinoma. epigenetics hsa-mir-34b Gastric Neoplasms 21960261 disease of cellular proliferation DOID:10534 C16 D013274 137215 The methylation-silenced expression of the miRNA could be reactivated in gastric cancer cells by treatment with demethylating drugs in a time-dependent manner.Analysis of the methylation status of these miRNAs showed that the upstream CpG-rich regions of mir-34b and mir-129-2 are frequently methylated in gastric cancer tissues compared to adjacent normal tissues, and their methylation status correlated inversely with their expression patterns. The expression of miR-34b and miR-129-3p was downregulated by DNA hypermethylation in primary gastric cancers, and the low expression was associated with poor clinicopathological features. epigenetics hsa-mir-34b Gastric Neoplasms 20924086 disease of cellular proliferation DOID:10534 C16 D013274 137215 These results suggest that miR-34b and miR-34c are novel tumor suppressors frequently silenced by DNA methylation in GC, that methylation of miR-34b/c is involved in an epigenetic field defect and that the methylation might be a predictive marker of GC risk. epigenetics hsa-mir-34b Gastric Neoplasms 22703336 disease of cellular proliferation DOID:10534 C16 D013274 137215 Methylation frequency of 5 miR CpG islands (miR-9-1, miR-9-3, miR-137, miR-34b, and miR-210) gradually increased while the proportion of methylated miR-200b gradually decreased during gastric carcinogenesis epigenetics hsa-mir-34c Gastric Neoplasms 23942619 disease of cellular proliferation DOID:10534 C16 D013274 137215 Our results suggest that methylation of miR-34b/c in the mucosa of the noncancerous gastric body may be a useful biomarker for predicting the risk of metachronous GC. epigenetics hsa-mir-34c Gastric Neoplasms 21914401 disease of cellular proliferation DOID:10534 C16 D013274 137215 The hypermethylation of miRNA-34b/c and miRNA-124a gene promoters may play a crucial role in the occurrence and development of gastric carcinoma. epigenetics hsa-mir-378a Gastric Neoplasms 23333942 disease of cellular proliferation DOID:10534 C16 D013274 137215 MicroRNA-195 and microRNA-378 mediate tumor growth suppression by epigenetical regulation in gastric cancer epigenetics hsa-mir-449a Gastric Neoplasms 24810364 disease of cellular proliferation DOID:10534 C16 D013274 137215 Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a. epigenetics hsa-mir-512 Gastric Neoplasms 19503096 disease of cellular proliferation DOID:10534 C16 D013274 137215 Chromatin remodeling at Alu repeats by epigenetic treatment activates silenced microRNA-512-5p with downregulation of Mcl-1 in human gastric cancer cells. epigenetics hsa-mir-9 Gastric Neoplasms 25270964 disease of cellular proliferation DOID:10534 C16 D013274 137215 Epigenetic silencing of miRNA-9 is correlated with promoter-proximal CpG island hypermethylation in gastric cancer in vitro and in vivo. epigenetics hsa-mir-9-1 Gastric Neoplasms 21931274 disease of cellular proliferation DOID:10534 C16 D013274 137215 In this study, we demonstrate that three independent genetic loci encoding for miR-9 (miR-9-1, miR-9-2 and miR-9-3) are simultaneously modified by DNA methylation in gastric cancer cells. Methylation-mediated silencing of these three miR-9 genes can be reactivated in gastric cancer cells through 5-Aza-dC treatment. epigenetics hsa-mir-9-1 Gastric Neoplasms 22703336 disease of cellular proliferation DOID:10534 C16 D013274 137215 Methylation frequency of 5 miR CpG islands (miR-9-1, miR-9-3, miR-137, miR-34b, and miR-210) gradually increased while the proportion of methylated miR-200b gradually decreased during gastric carcinogenesis epigenetics hsa-mir-9-2 Gastric Neoplasms 21931274 disease of cellular proliferation DOID:10534 C16 D013274 137215 In this study, we demonstrate that three independent genetic loci encoding for miR-9 (miR-9-1, miR-9-2 and miR-9-3) are simultaneously modified by DNA methylation in gastric cancer cells. Methylation-mediated silencing of these three miR-9 genes can be reactivated in gastric cancer cells through 5-Aza-dC treatment. epigenetics hsa-mir-9-3 Gastric Neoplasms 21931274 disease of cellular proliferation DOID:10534 C16 D013274 137215 In this study, we demonstrate that three independent genetic loci encoding for miR-9 (miR-9-1, miR-9-2 and miR-9-3) are simultaneously modified by DNA methylation in gastric cancer cells. Methylation-mediated silencing of these three miR-9 genes can be reactivated in gastric cancer cells through 5-Aza-dC treatment. epigenetics hsa-mir-9-3 Gastric Neoplasms 22703336 disease of cellular proliferation DOID:10534 C16 D013274 137215 Methylation frequency of 5 miR CpG islands (miR-9-1, miR-9-3, miR-137, miR-34b, and miR-210) gradually increased while the proportion of methylated miR-200b gradually decreased during gastric carcinogenesis epigenetics hsa-mir-99a Gastric Neoplasms 24810364 disease of cellular proliferation DOID:10534 C16 D013274 137215 Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a. epigenetics hsa-mir-1-1 Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-1 Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-2 Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-124-3 Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-148a Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-152 Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-18b Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-200a Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-208a Gastrointestinal Neoplasms 21327300 D37.9 D005770 Compared with the respective normal tissues, the predominant alteration in tumor tissues was increased methylation for the miRNAs 1-1, 124a-1, 124a-2, 124a-3, 148a, 152, and 18b; decreased methylation for 200a and 208a; epigenetics hsa-mir-212 Gastrointestinal Neoplasms 21053104 D37.9 D005770 The conclusion could be deduced from the study that decreased expression of miR-212 may be due to hypermethylation of CPI in gastric cancer cells, and miR-212 might act on the progression of gastric cancer through the potential target gene Myc. epigenetics hsa-mir-34c Gastrointestinal Neoplasms 20924086 D37.9 D005770 These results suggest that miR-34b and miR-34c are novel tumor suppressors frequently silenced by DNA methylation in GC, that methylation of miR-34b/c is involved in an epigenetic field defect and that the methylation might be a predictive marker of GC risk. epigenetics hsa-mir-122 Germ Cell Tumor 26497383 disease of cellular proliferation DOID:2994 Z85.43 D009373 273300 Cross platform analysis of methylation, miRNA and stem cell gene expression data in germ cell tumors highlights characteristic differences by tumor histology. epigenetics hsa-mir-302a Germ Cell Tumor 26497383 disease of cellular proliferation DOID:2994 Z85.43 D009373 273300 Cross platform analysis of methylation, miRNA and stem cell gene expression data in germ cell tumors highlights characteristic differences by tumor histology. epigenetics hsa-mir-302d Germ Cell Tumor 26497383 disease of cellular proliferation DOID:2994 Z85.43 D009373 273300 Cross platform analysis of methylation, miRNA and stem cell gene expression data in germ cell tumors highlights characteristic differences by tumor histology. epigenetics hsa-mir-371 Germ Cell Tumor 26497383 disease of cellular proliferation DOID:2994 Z85.43 D009373 273300 Cross platform analysis of methylation, miRNA and stem cell gene expression data in germ cell tumors highlights characteristic differences by tumor histology. epigenetics hsa-mir-373 Germ Cell Tumor 26497383 disease of cellular proliferation DOID:2994 Z85.43 D009373 273300 Cross platform analysis of methylation, miRNA and stem cell gene expression data in germ cell tumors highlights characteristic differences by tumor histology. epigenetics hsa-mir-101 Glioblastoma 29251856 D005909 HP:0100843 Studies of intragenic and distant intergenic alterations in DNA methylation will help elucidate the nature of epigenetic deregulation in glioblastoma epigenetics hsa-mir-137 Glioblastoma 26187071 D005909 HP:0100843 Direct transfection of miR-137 mimics is more effective than DNA demethylation of miR-137 promoter to augment anti-tumor mechanisms of delphinidin in human glioblastoma U87MG and LN18 cells. epigenetics hsa-mir-149 Glioblastoma 27783537 D005909 HP:0100843 MicroRNA-149 is epigenetically silenced tumor-suppressive microRNA, involved in cell proliferation and downregulation of AKT1 and cyclin D1 in human glioblastoma multiforme. epigenetics hsa-mir-153 Glioblastoma 27215075 D005909 HP:0100843 MiR-153 as a Tumor Suppressor in Glioblastoma Multiforme is Downregulated by DNA Methylation. epigenetics hsa-mir-181c Glioblastoma 26983574 D005909 HP:0100843 Epigenetic silencing of miR-181c by DNA methylation in glioblastoma cell lines. epigenetics hsa-mir-296 Glioblastoma 26898758 D005909 HP:0100843 We show that miR-296-5p expression is repressed in a DNA methylation-dependent manner under conditions that promote GBM cell stemness epigenetics hsa-let-7 Glioma 26463235 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 epigenetic modification is a crucial mechanism for controlling the expression of miR-126 in glioma. epigenetics hsa-mir-101 Glioma 25829251 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 MiR-101 reverses the hypomethylation of the LMO3 promoter in glioma cells. epigenetics hsa-mir-129-2 Glioma 25772485 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 MiR-129-2 functions as a tumor suppressor in glioma cells by targeting HMGB1 and is down-regulated by DNA methylation. epigenetics hsa-mir-185 Glioma 21962230 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 MiR-185 Targets the DNA Methyltransferases 1 and Regulates Global DNA Methylation in human glioma. epigenetics hsa-mir-20a Glioma 26337869 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 In summary, DNMT1 mediated chemosensitivity by reducing methylation of the microRNA-20a promoter in glioma cells. epigenetics hsa-mir-211 Glioma 23183822 disease of cellular proliferation DOID:3070 D005910 PS137800 HP:0009733 Epigenetic Regulation of miRNA-211 by MMP-9 Governs Glioma Cell Apoptosis,Chemosensitivity and Radiosensitivity epigenetics hsa-mir-1 Heart Diseases [unspecific] 28209718 I51.9 D006333 Demethylation of H3K27 Is Essential for the Induction of Direct Cardiac Reprogramming by miR Combo. epigenetics hsa-mir-133 Heart Diseases [unspecific] 28209718 I51.9 D006333 Demethylation of H3K27 Is Essential for the Induction of Direct Cardiac Reprogramming by miR Combo. epigenetics hsa-mir-208 Heart Diseases [unspecific] 28209718 I51.9 D006333 Demethylation of H3K27 Is Essential for the Induction of Direct Cardiac Reprogramming by miR Combo. epigenetics hsa-mir-499 Heart Diseases [unspecific] 28209718 I51.9 D006333 Demethylation of H3K27 Is Essential for the Induction of Direct Cardiac Reprogramming by miR Combo. epigenetics hsa-mir-210 Helicobacter pylori Infection 25187177 B96.81 D016480 600263 HP:0005202 Epigenetic silencing of miR-210 increases the proliferation of gastric epithelium during chronic Helicobacter pylori infection. epigenetics hsa-mir-148 Hematologic Neoplasms 26314468 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 This article summarizes the expression of miR-148/152 family in hematological malignancies, aiming at expounding the signicance of relationship between DNA methylation modification and microRNA. epigenetics hsa-mir-149 Hematologic Neoplasms 28035377 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 Histone deacetylases meet microRNA-associated MMP-9 expression regulation in glucocorticoid-sensitive and -resistant cell lines. epigenetics hsa-mir-152 Hematologic Neoplasms 26314468 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 This article summarizes the expression of miR-148/152 family in hematological malignancies, aiming at expounding the signicance of relationship between DNA methylation modification and microRNA. epigenetics hsa-mir-497 Hematologic Neoplasms 27075177 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 Strikingly, low-dose decitabine was able to augment chemosensitivity in cancer stem cells, likely by the upregulation of miRNA-497 epigenetics hsa-mir-520c Hematologic Neoplasms 28035377 disease of cellular proliferation DOID:2531 C96.9 D019337 HP:0004377 Histone deacetylases meet microRNA-associated MMP-9 expression regulation in glucocorticoid-sensitive and -resistant cell lines. epigenetics hsa-mir-101-1 Hepatitis B Virus Infection 23124077 disease by infectious agent DOID:2043 B16/18 D006509 610424 miR-101 is down-regulated by the hepatitis B virus x protein and induces aberrant DNA methylation by targeting DNA methyltransferase 3A epigenetics hsa-mir-101-2 Hepatitis B Virus Infection 23124077 disease by infectious agent DOID:2043 B16/18 D006509 610424 miR-101 is down-regulated by the hepatitis B virus x protein and induces aberrant DNA methylation by targeting DNA methyltransferase 3A epigenetics hsa-mir-205 Hepatitis B Virus Infection 24339740 disease by infectious agent DOID:2043 B16/18 D006509 610424 Hepatitis B virus X protein inhibits tumor suppressor miR-205 through inducing hypermethylation of miR-205 promoter to enhance carcinogenesis. epigenetics hsa-mir-200 Hepatoblastoma 24122292 disease of cellular proliferation DOID:687 C22.2 D018197 HP:0002884 The strong correlation between expression and DNA methylation suggests a major role for this epigenetic mark in the regulation of the miR-141-200c locus. epigenetics hsa-mir-205 Hepatoblastoma 24122292 disease of cellular proliferation DOID:687 C22.2 D018197 HP:0002884 The strong correlation between expression and DNA methylation suggests a major role for this epigenetic mark in the regulation of the miR-141-200c locus. epigenetics hsa-mir-1286 Human Papilloma Virus Infection 23732000 B97.7 D027383 We found hypermethylation of miR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 may have some relationship with HPV infection in cervical cell lines. epigenetics hsa-mir-1287 Human Papilloma Virus Infection 23732000 B97.7 D027383 We found hypermethylation of miR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 may have some relationship with HPV infection in cervical cell lines. epigenetics hsa-mir-1290 Human Papilloma Virus Infection 23732000 B97.7 D027383 We found hypermethylation of miR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 may have some relationship with HPV infection in cervical cell lines. epigenetics hsa-mir-432 Human Papilloma Virus Infection 23732000 B97.7 D027383 We found hypermethylation of miR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 may have some relationship with HPV infection in cervical cell lines. epigenetics hsa-mir-641 Human Papilloma Virus Infection 23732000 B97.7 D027383 We found hypermethylation of miR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 may have some relationship with HPV infection in cervical cell lines. epigenetics hsa-mir-95 Human Papilloma Virus Infection 23732000 B97.7 D027383 We found hypermethylation of miR-432, miR-1286, miR-641, miR-1290, miR-1287 and miR-95 may have some relationship with HPV infection in cervical cell lines. epigenetics hsa-mir-181b-1 Inflammation 20797623 D007249 miR-181b-1:STAT3 activation of miR-21 and miR-181b-1 via PTEN and CYLD are part of the epigenetic switch linking inflammation to cancer epigenetics hsa-mir-21 Inflammation 20797623 D007249 miR-21:STAT3 activation of miR-21 and miR-181b-1 via PTEN and CYLD are part of the epigenetic switch linking inflammation to cancer epigenetics hsa-mir-29a Influenza 22072783 respiratory system disease DOID:8469 J09-J11 D007251 614680 Epigenetic Changes Mediated by miR29 Activate Cyclooxygenase-2 and Interferon Production during Viral Infection. epigenetics hsa-mir-34b Leukemia 26524015 C95 D007938 613065 HP:0001909 CpG island methylation of miR-34b promoter region in leukemia cell lines can decrease the expression levels of miR-34b, which is also the reason why miR-34b can reduce the inhibition of cell proliferation, thus miR-34b might be a tumor suppressor gene involved in the regulation of leukemia. epigenetics hsa-mir-34b Leukemia 25582471 C95 D007938 613065 HP:0001909 The hypermethylation of promoter leads to decrease in the expression levels of miR-34b in leukemia cell lines, which attenuate mechanism of proliferative inhibition may be one of the reasons of occurrence or development of childhood leukemia. epigenetics hsa-mir-22 Leukemia, Lymphoblastic, Acute 19807731 disease of cellular proliferation DOID:9952 C91.0 D054198 247640 HP:0006721 Thus, accumulation of H3K27triM independent of promoter DNA methylation may be a novel epigenetic mechanism for MIR22 silencing in ALL. epigenetics hsa-mir-15a Leukemia, Lymphocytic, Chronic, B-Cell 22096249 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Histone deacetylases mediate the silencing of miR-15a, miR-16 and miR-29b in chronic lymphocytic leukemia. epigenetics hsa-mir-16-1 Leukemia, Lymphocytic, Chronic, B-Cell 22096249 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Histone deacetylases mediate the silencing of miR-15a, miR-16 and miR-29b in chronic lymphocytic leukemia. epigenetics hsa-mir-16-2 Leukemia, Lymphocytic, Chronic, B-Cell 22096249 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Histone deacetylases mediate the silencing of miR-15a, miR-16 and miR-29b in chronic lymphocytic leukemia. epigenetics hsa-mir-214 Leukemia, Lymphocytic, Chronic, B-Cell 25361012 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 miR-26a and miR-214 down-regulate expression of the PTEN gene in chronic lymphocytic leukemia, but not PTEN mutation or promoter methylation. epigenetics hsa-mir-26a Leukemia, Lymphocytic, Chronic, B-Cell 25361012 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 miR-26a and miR-214 down-regulate expression of the PTEN gene in chronic lymphocytic leukemia, but not PTEN mutation or promoter methylation. epigenetics hsa-mir-29b-1 Leukemia, Lymphocytic, Chronic, B-Cell 22096249 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Histone deacetylases mediate the silencing of miR-15a, miR-16 and miR-29b in chronic lymphocytic leukemia. epigenetics hsa-mir-29b-2 Leukemia, Lymphocytic, Chronic, B-Cell 22096249 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Histone deacetylases mediate the silencing of miR-15a, miR-16 and miR-29b in chronic lymphocytic leukemia. epigenetics hsa-mir-34 Leukemia, Lymphocytic, Chronic, B-Cell 24686393 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 microRNA-34b/c on chromosome 11q23 is aberrantly methylated in chronic lymphocytic leukemia. epigenetics hsa-mir-34a Leukemia, Lymphocytic, Chronic, B-Cell 24559316 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Taken together, miR-34b/c is a tumor suppressor miRNA frequently methylated, and hence silenced in CLL. Together with DAPK1 methylation, miR-34b/c methylation is implicated in the disruption of the TP53-centered tumor suppressor network. Moreover, the association of miRNA methylation warrants further study. epigenetics hsa-mir-34b Leukemia, Lymphocytic, Chronic, B-Cell 24559316 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Taken together, miR-34b/c is a tumor suppressor miRNA frequently methylated, and hence silenced in CLL. Together with DAPK1 methylation, miR-34b/c methylation is implicated in the disruption of the TP53-centered tumor suppressor network. Moreover, the association of miRNA methylation warrants further study. epigenetics hsa-mir-34b Leukemia, Lymphocytic, Chronic, B-Cell 24686393 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 microRNA-34b/c on chromosome 11q23 is aberrantly methylated in chronic lymphocytic leukemia. epigenetics hsa-mir-34c Leukemia, Lymphocytic, Chronic, B-Cell 24686393 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 microRNA-34b/c on chromosome 11q23 is aberrantly methylated in chronic lymphocytic leukemia. epigenetics hsa-mir-34c Leukemia, Lymphocytic, Chronic, B-Cell 24559316 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Taken together, miR-34b/c is a tumor suppressor miRNA frequently methylated, and hence silenced in CLL. Together with DAPK1 methylation, miR-34b/c methylation is implicated in the disruption of the TP53-centered tumor suppressor network. Moreover, the association of miRNA methylation warrants further study. epigenetics hsa-mir-9 Leukemia, Lymphocytic, Chronic, B-Cell 24373626 disease of cellular proliferation DOID:1040 C91.1 D015451 151400 HP:0005550 Of the miR-9 family, miR-9-3 is a tumor suppressor miRNA relatively frequently methylated, and hence silenced in CLL; whereas miR-9-1 methylation is rare in CLL. The role of miR-9-3 methylation in the constitutive activation of NFκB signaling pathway in CLL warrants further study. epigenetics hsa-let-7a-3 Leukemia, Myeloid, Acute 24703161 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 MicroRNA let-7a-3 gene methylation is associated with karyotyping, CEBPA promoter methylation, and survival in acute myeloid leukemia. epigenetics hsa-mir-15a Leukemia, Myeloid, Acute 24885794 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 The DLEU2 locus and embedded miRNA cluster miR-15a/16-1 is commonly deleted in adult cancers and shown to induce leukaemogenesis, however in paediatric AML we found the region to be transcriptionally repressed. In combination, our data highlights the utility of interrogating DNA methylation and microRNA in combination with underlying genetic status to provide novel insights into AML biology. epigenetics hsa-mir-16-1 Leukemia, Myeloid, Acute 24885794 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 The DLEU2 locus and embedded miRNA cluster miR-15a/16-1 is commonly deleted in adult cancers and shown to induce leukaemogenesis, however in paediatric AML we found the region to be transcriptionally repressed. In combination, our data highlights the utility of interrogating DNA methylation and microRNA in combination with underlying genetic status to provide novel insights into AML biology. epigenetics hsa-mir-17 Leukemia, Myeloid, Acute 21897363 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 We propose that upon macrophage differentiation PU.1 represses the miR-17-92 cluster promoter by an Egr-2/Jarid1b-mediated H3K4 demethylation mechanism whose deregulation may contribute to leukaemic states. epigenetics hsa-mir-18 Leukemia, Myeloid, Acute 21897363 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 We propose that upon macrophage differentiation PU.1 represses the miR-17-92 cluster promoter by an Egr-2/Jarid1b-mediated H3K4 demethylation mechanism whose deregulation may contribute to leukaemic states. epigenetics hsa-mir-193a Leukemia, Myeloid, Acute 21399664 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 MicroRNA-193a represses c-kit expression and functions as a methylation-silenced tumor suppressor in acute myeloid leukemia. epigenetics hsa-mir-193a Leukemia, Myeloid, Acute 23223432 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Epigenetic silencing of microRNA-193a contributes to leukemogenesis in t(8;21)acute myeloid leukemia by activating the PTEN/PI3K signal pathway epigenetics hsa-mir-19a Leukemia, Myeloid, Acute 21897363 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 We propose that upon macrophage differentiation PU.1 represses the miR-17-92 cluster promoter by an Egr-2/Jarid1b-mediated H3K4 demethylation mechanism whose deregulation may contribute to leukaemic states. epigenetics hsa-mir-19b-1 Leukemia, Myeloid, Acute 21897363 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 We propose that upon macrophage differentiation PU.1 represses the miR-17-92 cluster promoter by an Egr-2/Jarid1b-mediated H3K4 demethylation mechanism whose deregulation may contribute to leukaemic states. epigenetics hsa-mir-200 Leukemia, Myeloid, Acute 27756750 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 epigenetic silencing of the miR-200 family microRNAs affects ZEB2 expression epigenetics hsa-mir-203 Leukemia, Myeloid, Acute 21323860 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 The frequent hsa-miR-203 methylation in lymphoid malignancies suggested a pathogenetic role of hsa-miR-203 methylation. epigenetics hsa-mir-20a Leukemia, Myeloid, Acute 21897363 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 We propose that upon macrophage differentiation PU.1 represses the miR-17-92 cluster promoter by an Egr-2/Jarid1b-mediated H3K4 demethylation mechanism whose deregulation may contribute to leukaemic states. epigenetics hsa-mir-24-1 Leukemia, Myeloid, Acute 21544199 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 miR-124-1 is epigenetically inactivated in Haematological Malignancies. epigenetics hsa-mir-29b-1 Leukemia, Myeloid, Acute 19211935 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 miR-29b: induces global DNA hypomethylation and tumor suppressor gene re-expression in acute myeloid leukemia by targeting directly DNMT3A and 3B and indirectly DNMT1 epigenetics hsa-mir-29b-1 Leukemia, Myeloid, Acute 23178755 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Increased anti-leukemic activity of decitabine via AR-42-induced upregulation of miR-29b: a novel epigenetic-targeting approach in acute myeloid leukemia epigenetics hsa-mir-29b-2 Leukemia, Myeloid, Acute 19211935 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 miR-29b: induces global DNA hypomethylation and tumor suppressor gene re-expression in acute myeloid leukemia by targeting directly DNMT3A and 3B and indirectly DNMT1 epigenetics hsa-mir-29b-2 Leukemia, Myeloid, Acute 23178755 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Increased anti-leukemic activity of decitabine via AR-42-induced upregulation of miR-29b: a novel epigenetic-targeting approach in acute myeloid leukemia epigenetics hsa-mir-663 Leukemia, Myeloid, Acute 23870168 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 Expression of miR-663 was significantly lower in pediatric AML cells compared to NBM controls; furthermore, a high frequency of miR-663 promoter hypermethylation was observed in both AML cell lines and pediatric AML samples.Inactivation of miR-663 by promoter hypermethylation could be affected by 5-Aza demethylation. These findings suggest that hypermethylation of the miR-663 promoter may be an early event in the development of pediatric AML. epigenetics hsa-mir-720 Leukemia, Myeloid, Acute 25417880 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 The expression of miR-720 in AML patients reduced significantly, and DNA methylation-mediated epigenetic silencing of miR-720 contributed to maintain the malignant characteristics of AML. epigenetics hsa-mir-92-1 Leukemia, Myeloid, Acute 21897363 disease of cellular proliferation DOID:9119 C92.0 D015470 HP:0004820 We propose that upon macrophage differentiation PU.1 represses the miR-17-92 cluster promoter by an Egr-2/Jarid1b-mediated H3K4 demethylation mechanism whose deregulation may contribute to leukaemic states. epigenetics hsa-mir-203 Leukemia, Myeloid, Acute, Pediatric 24103876 C92.0 miR-203 may not be regulated with methylation mechanism in pediatric acute leukemia. miR- 203 may be a protooncogene involved in the formation of pediatric acute leukemia and ALL. Further analyses indicated that high expression of miR-203 may be associated with poor prognosis of pediatric ALL and acute leukemia. epigenetics hsa-mir-21 Leukemia, Myeloid, Chronic 25575817 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 RBP2 epigenetically downregulated miR-21 in blast transformation of CML. epigenetics hsa-mir-369 Leukemia, Myeloid, Chronic 22089542 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 The CpG islands in the upstream regions of miR-663, miR-369, miR-615, and miR-410, and promoter activity was detected in the upstream region of pre-miR-663. We found that a decrease in methylation of a CpG island could up-regulate the expression of miR-663, suggesting that miR-663 could be regulated by DNA methylation. epigenetics hsa-mir-378 Leukemia, Myeloid, Chronic 26913395 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 Methylation of miR-378 in Chronic Myeloid Leukemia. epigenetics hsa-mir-410 Leukemia, Myeloid, Chronic 22089542 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 The CpG islands in the upstream regions of miR-663, miR-369, miR-615, and miR-410, and promoter activity was detected in the upstream region of pre-miR-663. We found that a decrease in methylation of a CpG island could up-regulate the expression of miR-663, suggesting that miR-663 could be regulated by DNA methylation. epigenetics hsa-mir-615 Leukemia, Myeloid, Chronic 22089542 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 The CpG islands in the upstream regions of miR-663, miR-369, miR-615, and miR-410, and promoter activity was detected in the upstream region of pre-miR-663. We found that a decrease in methylation of a CpG island could up-regulate the expression of miR-663, suggesting that miR-663 could be regulated by DNA methylation. epigenetics hsa-mir-663a Leukemia, Myeloid, Chronic 22089542 disease of cellular proliferation DOID:8552 C92.1 D015464 HP:0005506 The CpG islands in the upstream regions of miR-663, miR-369, miR-615, and miR-410, and promoter activity was detected in the upstream region of pre-miR-663. We found that a decrease in methylation of a CpG island could up-regulate the expression of miR-663, suggesting that miR-663 could be regulated by DNA methylation. epigenetics hsa-mir-34a Leukemia, Promyelocytic, Acute 24811488 disease of cellular proliferation DOID:0060318 C92.4 D015473 612376 HP:0004836 Epigenetic inactivation of DAPK1, p14ARF, mir-34a and -34b/c in acute promyelocytic leukaemia. epigenetics hsa-mir-34b Leukemia, Promyelocytic, Acute 24811488 disease of cellular proliferation DOID:0060318 C92.4 D015473 612376 HP:0004836 Epigenetic inactivation of DAPK1, p14ARF, mir-34a and -34b/c in acute promyelocytic leukaemia. epigenetics hsa-mir-34c Leukemia, Promyelocytic, Acute 24811488 disease of cellular proliferation DOID:0060318 C92.4 D015473 612376 HP:0004836 Epigenetic inactivation of DAPK1, p14ARF, mir-34a and -34b/c in acute promyelocytic leukaemia. epigenetics hsa-mir-128a Leukemia, T-Cell 24316133 disease of cellular proliferation DOID:715 C91.5 D015458 Epigenetic regulation of microRNA-128a expression contributes to the apoptosis-resistance of human T-cell leukaemia jurkat cells by modulating expression of fas-associated protein with death domain (FADD). epigenetics hsa-mir-143 Leukemia-Lymphoma, Precursor T-Cell Lymphoblastic 21706045 disease of cellular proliferation DOID:5599 C83.5 D054218 Methylation-mediated repression of microRNA-143 enhances MLL-AF4 oncogene expression. epigenetics hsa-mir-378a Liver Cirrhosis 27855367 endocrine system disease DOID:5082 K74 D008103 215600 HP:0001394 The Epigenetically-Regulated microRNA-378a Targets TGF-β2 in TGF-β1-Treated Hepatic Stellate Cells. epigenetics hsa-mir-29b Liver Fibrosis 24138392 K74 D008103 Curcumin up-regulates phosphatase and tensin homologue deleted on chromosome 10 through microRNA-mediated control of DNA methylation--a novel mechanism suppressing liver fibrosis. epigenetics hsa-mir-373 Liver Neoplasms 21706058 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 Thus, histone deacetylation of CDH1 and downregulation of miR-373, together with the previously demonstrated hypermethylation of CDH1 by HBx, may be important for the understanding of HBV-related carcinogenesis. epigenetics hsa-let-7b Liver Neoplasms 22683924 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 Downregulation of HMGA2 by the pan-deacetylase inhibitor panobinostat is dependent on hsa-let-7b expression in liver cancer cell lines. epigenetics hsa-mir-491 Liver Neoplasms 24680928 disease of cellular proliferation DOID:916 C22.0 D008113 HP:0002896 Arsenic trioxide attenuates the invasion potential of human liver cancer cells through the demethylation-activated microRNA-491. epigenetics hsa-mir-214 Lung Fibrosis 24122720 respiratory system disease DOID:3770 J84.10 D011658 178500 Stable decreases in miR-124 expression contribute to an epigenetically reprogrammed, highly proliferative, migratory, and inflammatory phenotype of hypertensive pulmonary adventitial fibroblasts. Thus, therapies directed at restoring miR-124 function, including histone deacetylase inhibitors,should be investigated. epigenetics hsa-mir-101 Lung Neoplasms 25210796 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Restoration of miR-101 suppresses lung tumorigenesis through inhibition of DNMT3a-dependent DNA methylation. epigenetics hsa-mir-1258 Lung Neoplasms 24450160 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Novel miRNA genes methylated in lung tumors. epigenetics hsa-mir-127 Lung Neoplasms 24665010 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Epigenetic analysis of microRNA genes in tumors from surgically resected lung cancer patients and association with survival. epigenetics hsa-mir-129-2 Lung Neoplasms 26081366 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Epigenetic regulation of miR-129-2 and its effects on the proliferation and invasion in lung cancer cells. epigenetics hsa-mir-137 Lung Neoplasms 24450160 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Novel miRNA genes methylated in lung tumors. epigenetics hsa-mir-148a Lung Neoplasms 20431052 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 miR-148a:The silencing of microRNA 148a production by DNA hypermethylation is an early event in pancreatic carcinogenesis epigenetics hsa-mir-182 Lung Neoplasms 25975295 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 DNA methylation occurs in the miR-182 promoter region in lung cancer cell lines. This methylation can regulate the expression level of miR-182.Further study must be conducted to explore the function of miR-182 promoter methylation in lung cancer occurrence and development. epigenetics hsa-mir-200 Lung Neoplasms 28698146 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Epigenetic regulation of epithelial-mesenchymal transition by KDM6A histone demethylase in lung cancer cells. epigenetics hsa-mir-29a Lung Neoplasms 17890317 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 mir-29 family (29a,b,c) reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B. epigenetics hsa-mir-29b Lung Neoplasms 17890317 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 MicroRNA-29 family reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B. epigenetics hsa-mir-29b-1 Lung Neoplasms 17890317 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 mir-29 family (29a,b,c) reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B. epigenetics hsa-mir-29c Lung Neoplasms 17890317 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 mir-29 family (29a,b,c) reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B. epigenetics hsa-mir-375 Lung Neoplasms 24450160 disease of cellular proliferation DOID:1324 C34.1-.3 D008175 HP:0100526 Novel miRNA genes methylated in lung tumors. epigenetics hsa-mir-155 Lymphoma 27110708 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 DNA methylation regulates miR-155 expression. epigenetics hsa-mir-203 Lymphoma 21454413 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 Epigenetic silencing of microRNA-203 dysregulates ABL1 expression and drives Helicobacter-associated gastric lymphomagenesis. epigenetics hsa-mir-24-1 Lymphoma 21544199 disease of cellular proliferation DOID:0060058 C85.9 D008223 HP:0002665 miR-124-1 is epigenetically inactivated in Haematological Malignancies. epigenetics hsa-mir-146a Lymphoma, Burkitt 23528241 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 We concluded that similarly to the promoters of protein coding genes, both DNA methylation and histone modifications contribute to the host cell dependent expression of miR-146a. epigenetics hsa-mir-29a Lymphoma, Burkitt 29318382 disease of cellular proliferation DOID:8584 C83.7 D002051 113970 HP:0030080 methylation-mediated miR-29 epigenetic silencing may occur during BL development epigenetics hsa-mir-155 Lymphoma, Non-Hodgkin 25211095 disease of cellular proliferation DOID:0060060 C85.9 D008228 605027 HP:0012539 Methylation of miR-155-3p in mantle cell lymphoma and other non-Hodgkin's lymphomas. epigenetics hsa-mir-142 Lymphoma, T-Cell 25405321 disease of cellular proliferation DOID:0050749 C84.4 D016399 186960 HP:0012190 These results reveal a subgroup-specific epigenetically regulated microRNA signatures for MFt and CD30+ cALCL patients. epigenetics hsa-mir-146a Lymphoma, T-Cell 25405321 disease of cellular proliferation DOID:0050749 C84.4 D016399 186960 HP:0012190 These results reveal a subgroup-specific epigenetically regulated microRNA signatures for MFt and CD30+ cALCL patients. epigenetics hsa-mir-155 Lymphoma, T-Cell 25405321 disease of cellular proliferation DOID:0050749 C84.4 D016399 186960 HP:0012190 These results reveal a subgroup-specific epigenetically regulated microRNA signatures for MFt and CD30+ cALCL patients. epigenetics hsa-mir-181b Lymphoma, T-Cell 25405321 disease of cellular proliferation DOID:0050749 C84.4 D016399 186960 HP:0012190 These results reveal a subgroup-specific epigenetically regulated microRNA signatures for MFt and CD30+ cALCL patients. epigenetics hsa-mir-21 Lymphoma, T-Cell 25405321 disease of cellular proliferation DOID:0050749 C84.4 D016399 186960 HP:0012190 These results reveal a subgroup-specific epigenetically regulated microRNA signatures for MFt and CD30+ cALCL patients. epigenetics hsa-mir-199b Medulloblastoma 22411914 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 The micro-RNA 199b-5p regulatory circuit involves Hes1, CD15, and epigenetic modifications in medulloblastoma. epigenetics hsa-mir-9 Medulloblastoma 24346283 disease of cellular proliferation DOID:0050902 C71.6 D008527 155255 HP:0002885 microRNA-9 is a methylation-silenced tumour suppressor that could be a potential candidate predictive marker for poor prognosis of medulloblastoma. epigenetics hsa-mir-124a Melanoma 24303550 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Epigenetic regulation of melanoma tumor suppressor miRNA-124a. epigenetics hsa-mir-125b Melanoma 24118912 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 the reduction in miR-125b expression in pigmented cells was at least partially due to the hypermethylation of the MIR125B-1 promoter, and miR-125b expression was regulated by intracellular cAMP levels. epigenetics hsa-mir-203 Melanoma 26225581 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 DNA methylation contributes toward silencing of antioncogenic microRNA-203 in human and canine melanoma cells. epigenetics hsa-mir-211 Melanoma 27237979 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 DNMT1 mediated promoter methylation is a mechanism of miRNA suppression in melanoma epigenetics hsa-mir-31 Melanoma 22948084 disease of cellular proliferation DOID:1909 C43.9 D008545 155601 HP:0002861 Genetic and epigenetic loss of microRNA-31 leads to feed-forward expression of EZH2 in melanoma. epigenetics hsa-mir-34b Mesothelioma 21673066 disease of cellular proliferation DOID:1790 C45.9 C562839 156240 HP:0100001 Epigenetic Silencing of MicroRNA-34b/c Plays an Important Role in the Pathogenesis of Malignant Pleural Mesothelioma. epigenetics hsa-mir-34c Mesothelioma 21673066 disease of cellular proliferation DOID:1790 C45.9 C562839 156240 HP:0100001 Epigenetic Silencing of MicroRNA-34b/c Plays an Important Role in the Pathogenesis of Malignant Pleural Mesothelioma. epigenetics hsa-mir-155 Multiple Myeloma 25497370 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 DNA methylation contributes to miR-155 expression in myeloma cells. Interestingly, the survival data showed an association between miR-155 expression and outcome of MM. epigenetics hsa-mir-203 Multiple Myeloma 21707582 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 MIR203 is epigeneticlly silenced in multiple myeloma. epigenetics hsa-mir-24-1 Multiple Myeloma 21544199 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 miR-124-1 is epigenetically inactivated in Haematological Malignancies. epigenetics hsa-mir-29b-1 Multiple Myeloma 23100393 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 DNA-demethylating and anti-tumor activity of synthetic miR-29b mimics in multiple myeloma epigenetics hsa-mir-29b-2 Multiple Myeloma 23100393 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 DNA-demethylating and anti-tumor activity of synthetic miR-29b mimics in multiple myeloma epigenetics hsa-mir-342 Multiple Myeloma 29242101 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 Epigenetic silencing of EVL/miR-342 in multiple myeloma epigenetics hsa-mir-9-1 Multiple Myeloma 25855800 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 Hypermethylation of miR-9-3 and miR-9-1 is tumour-specific in MM,leading to reversible miRNA silencing. Frequent methylation of miR-9-3 and miR-9-1 in cell lines, but not in primary samples, may be acquired during in vitro culture, and indicates an unimportant role of miR-9 methylation in myelomagenesis. epigenetics hsa-mir-9-3 Multiple Myeloma 25855800 disease of cellular proliferation DOID:9538 D009101 254500 HP:0006775 Hypermethylation of miR-9-3 and miR-9-1 is tumour-specific in MM,leading to reversible miRNA silencing. Frequent methylation of miR-9-3 and miR-9-1 in cell lines, but not in primary samples, may be acquired during in vitro culture, and indicates an unimportant role of miR-9 methylation in myelomagenesis. epigenetics hsa-mir-124-1 Myelodysplastic Syndromes 20448201 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 miRNA-124:Methylation and silencing of miRNA-124 by EVI1 and self-renewal exhaustion of hematopoietic stem cells in murine myelodysplastic syndrome epigenetics hsa-mir-124-2 Myelodysplastic Syndromes 20448201 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 miRNA-124:Methylation and silencing of miRNA-124 by EVI1 and self-renewal exhaustion of hematopoietic stem cells in murine myelodysplastic syndrome epigenetics hsa-mir-124-3 Myelodysplastic Syndromes 20448201 disease of cellular proliferation DOID:0050908 D46.9 D009190 614286 HP:0002863 miRNA-124:Methylation and silencing of miRNA-124 by EVI1 and self-renewal exhaustion of hematopoietic stem cells in murine myelodysplastic syndrome epigenetics hsa-mir-126 Myeloma 24875904 C90.0 D009101 254500 TNFα in the marrow microenvironment led to RANKL demethylation and re-expression in myeloma cells through DNMT1 repression and upregulation of miR-126-3p and miR-140, both known to repress DNMT1 translation. epigenetics hsa-mir-140 Myeloma 24875904 C90.0 D009101 254500 TNFα in the marrow microenvironment led to RANKL demethylation and re-expression in myeloma cells through DNMT1 repression and upregulation of miR-126-3p and miR-140, both known to repress DNMT1 translation. epigenetics hsa-mir-375 Myeloproliferative Neoplasms 25666256 disease of cellular proliferation DOID:2226 D47.1 616871 Epigenetic deregulated miR-375 contributes to the constitutive activation of JAK2/STAT signaling in myeloproliferative neoplasm. epigenetics hsa-let-7 Neoplasms [unspecific] 26303212 C80.1 D009369 Impact of Histone Deacetylase Inhibitors on microRNA Expression and Cancer Therapy: A Review. epigenetics hsa-let-7a-3 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. epigenetics hsa-mir-105 Neoplasms [unspecific] 25089631 C80.1 D009369 A novel cancer-germline transcript carrying pro-metastatic miR-105 and TET-targeting miR-767 induced by DNA hypomethylation in tumors. epigenetics hsa-mir-106a Neoplasms [unspecific] 26303212 C80.1 D009369 Impact of Histone Deacetylase Inhibitors on microRNA Expression and Cancer Therapy: A Review. epigenetics hsa-mir-106b Neoplasms [unspecific] 26303212 C80.1 D009369 Impact of Histone Deacetylase Inhibitors on microRNA Expression and Cancer Therapy: A Review. epigenetics hsa-mir-125b Neoplasms [unspecific] 26354435 C80.1 D009369 Taken together, our results demonstrated that miR-125b mediates PAR2-induced cancer cell migration by targeting Gab2 and that NSun2-dependent RNA methylation contributes to the down-regulation of miR-125b by PAR2 signaling. epigenetics hsa-mir-126 Neoplasms [unspecific] 19116145 C80.1 D009369 miR-126: a tumor supressor: Epigenetic therapy upregulates the tumor suppressor microRNA-126 and its host gene EGFL7 epigenetics hsa-mir-137 Neoplasms [unspecific] 26066330 C80.1 D009369 We also found that miR-137 and its host gene are epigenetically silenced in human cancer specimens and cell lines.These results support the development and testing of microRNA-based therapies (in particular based on restoring miR-137 levels) for targeting the oncogenic family of p160 SRCs in cancer. epigenetics hsa-mir-15a Neoplasms [unspecific] 26303212 C80.1 D009369 Impact of Histone Deacetylase Inhibitors on microRNA Expression and Cancer Therapy: A Review. epigenetics hsa-mir-16 Neoplasms [unspecific] 26303212 C80.1 D009369 Impact of Histone Deacetylase Inhibitors on microRNA Expression and Cancer Therapy: A Review. epigenetics hsa-mir-17 Neoplasms [unspecific] 26303212 C80.1 D009369 Impact of Histone Deacetylase Inhibitors on microRNA Expression and Cancer Therapy: A Review. epigenetics hsa-mir-181b-1 Neoplasms [unspecific] 20797623 C80.1 D009369 miR-181b-1:STAT3 activation of miR-21 and miR-181b-1 via PTEN and CYLD are part of the epigenetic switch linking inflammation to cancer epigenetics hsa-mir-19b Neoplasms [unspecific] 26303212 C80.1 D009369 Impact of Histone Deacetylase Inhibitors on microRNA Expression and Cancer Therapy: A Review. epigenetics hsa-mir-200 Neoplasms [unspecific] 25178837 C80.1 D009369 Zeb1 and Snail1 engage miR-200f transcriptional and epigenetic regulation during EMT. epigenetics hsa-mir-200b Neoplasms [unspecific] 21292642 C80.1 D009369 Depletion of miR-200 in arsenite-transformed cells involved induction of the EMT-inducing transcription factors ZEB1 (zinc-finger E-box-binding homeobox factor 1) and ZEB2 and increased methylation of miR-200 promoters. epigenetics hsa-mir-21 Neoplasms [unspecific] 20797623 C80.1 D009369 miR-21:STAT3 activation of miR-21 and miR-181b-1 via PTEN and CYLD are part of the epigenetic switch linking inflammation to cancer epigenetics hsa-mir-24-2 Neoplasms [unspecific] 25943634 C80.1 D009369 The conclusion drawn of hsa-miR-24-2 targeting the genes of cell survival correlated with the methylation profile and resultant transcription factor binding site gain or loss in support of absence of cell survival. epigenetics hsa-mir-29 Neoplasms [unspecific] 24096364 C80.1 D009369 The miR-29 family recurrently regulates active DNA demethylation pathway members TET1 and TDG. epigenetics hsa-mir-34a Neoplasms [unspecific] 18719384 C80.1 D009369 miR-34a: inactivation, Inactivation of miR-34a by aberrant CpG methylation in multiple types of cancer epigenetics hsa-mir-34b Neoplasms [unspecific] 18768788 C80.1 D009369 miR-34b: were found to undergo specific hypermethylation-associated silencing in cancer cells compared with normal tissues epigenetics hsa-mir-34b Neoplasms [unspecific] 22082000 C80.1 D009369 miR-34b/c were homozygously methylated in HEL cells but heterozygously in MEG-01. In HEL cells, homozygous miR-34b/c methylation was associated with miR silencing, and 5-aza-2'-deoxycytidine treatment led to re-expression of both miR-34b and miR-34c, consistent with that both miRs are under the regulation of the same promoter CpG island. miR-34a was heterozygously methylated in MEG-01 and K-562. miR-203 was completely unmethylated in K-562 and SET-2 but no MSP amplification was found in both HEL and MEG-01, suggestive of miR deletion. In primary samples, four each had miR-34b/c and -203 methylation, in which two had concomitant methylation of miR-34b/c and -203. miR-34a was methylated in one patient and none had methylation of miR-124-1. epigenetics hsa-mir-34b Neoplasms [unspecific] 25979762 C80.1 D009369 although results obtained by the different DNA methylation analysis techniques are largely comparable, an appropriate correction may be necessary for stringent comparison. epigenetics hsa-mir-34c Neoplasms [unspecific] 18768788 C80.1 D009369 miR-34c: were found to undergo specific hypermethylation-associated silencing in cancer cells compared with normal tissues epigenetics hsa-mir-34c Neoplasms [unspecific] 22082000 C80.1 D009369 miR-34b/c were homozygously methylated in HEL cells but heterozygously in MEG-01. In HEL cells, homozygous miR-34b/c methylation was associated with miR silencing, and 5-aza-2'-deoxycytidine treatment led to re-expression of both miR-34b and miR-34c, consistent with that both miRs are under the regulation of the same promoter CpG island. miR-34a was heterozygously methylated in MEG-01 and K-562. miR-203 was completely unmethylated in K-562 and SET-2 but no MSP amplification was found in both HEL and MEG-01, suggestive of miR deletion. In primary samples, four each had miR-34b/c and -203 methylation, in which two had concomitant methylation of miR-34b/c and -203. miR-34a was methylated in one patient and none had methylation of miR-124-1. epigenetics hsa-mir-34c Neoplasms [unspecific] 25979762 C80.1 D009369 although results obtained by the different DNA methylation analysis techniques are largely comparable, an appropriate correction may be necessary for stringent comparison. epigenetics hsa-mir-767 Neoplasms [unspecific] 25089631 C80.1 D009369 A novel cancer-germline transcript carrying pro-metastatic miR-105 and TET-targeting miR-767 induced by DNA hypomethylation in tumors. epigenetics hsa-mir-9-1 Neoplasms [unspecific] 18768788 C80.1 D009369 miR-9: were found to undergo specific hypermethylation-associated silencing in cancer cells compared with normal tissues epigenetics hsa-mir-9-2 Neoplasms [unspecific] 18768788 C80.1 D009369 miR-9: were found to undergo specific hypermethylation-associated silencing in cancer cells compared with normal tissues epigenetics hsa-mir-9-3 Neoplasms [unspecific] 18768788 C80.1 D009369 miR-9: were found to undergo specific hypermethylation-associated silencing in cancer cells compared with normal tissues epigenetics hsa-mir-21 Nervous System Diseases [unspecific] 28903050 C72.9 D009422 Changes in the Coding and Non-coding Transcriptome and DNA Methylome that Define the Schwann Cell Repair Phenotype after Nerve Injury. epigenetics hsa-mir-137 Neuroblastoma 25505154 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 an epigenetic mechanism involving miR-137-mediated EZH2 repression in RSV-induced apoptosis and tumor suppression of neuroblastoma, which would provide a key potential therapeutic target in neuroblastoma treatment. epigenetics hsa-mir-340 Neuroblastoma 22797059 disease of cellular proliferation DOID:769 C74.90 D009447 256700 HP:0003006 miR-340 is upregulated by demethylation of an upstream genomic region that occurs during the process of neuroblastoma cell differentiation induced by all-trans retinoic acid (ATRA). epigenetics hsa-mir-181a Neurodegenerative Diseases [unspecific] 27789312 D019636 HP:0002180 PPARβ/δ activation protects against corticosterone-induced ER stress in astrocytes by inhibiting the CpG hypermethylation of microRNA-181a. epigenetics hsa-mir-140 Osteoarthritis 26723856 musculoskeletal system disease DOID:8398 M19.9 D010003 165720 HP:0002758 Some miRNA have also been identified and more extensively characterized, such as delineation of the role played by miR-140 in chondrogenesis, followed by the discovery of numerous miRNA potentially involved in the epigenetic regulation of osteoarthritic disease. epigenetics hsa-mir-148a Osteoporosis 27900532 musculoskeletal system disease DOID:11476 M80 D010024 166710 HP:0000939 MiR-148a the epigenetic regulator of bone homeostasis is increased in plasma of osteoporotic postmenopausal women. epigenetics hsa-mir-127 Osteosarcoma 22957032 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Treatment with 4-phenylbutyrate increased acetylation of histones associated with 14q32 miRNAs, but interestingly, robust restoration of 14q32 miRNA expression, attenuation of cMYC expression, and induction of apoptosis required concomitant treatment with 5-Azacytidine, an inhibitor of DNA methylation. combination of these chromatin-modifying drugs may be a useful adjuvant in the treatment of rapidly progressive osteosarcoma. epigenetics hsa-mir-328 Osteosarcoma 25605016 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 the role of RESV-induced molecular and epigenetic regulation in suppressing tumor metastasis. epigenetics hsa-mir-411 Osteosarcoma 22957032 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Treatment with 4-phenylbutyrate increased acetylation of histones associated with 14q32 miRNAs, but interestingly, robust restoration of 14q32 miRNA expression, attenuation of cMYC expression, and induction of apoptosis required concomitant treatment with 5-Azacytidine, an inhibitor of DNA methylation. combination of these chromatin-modifying drugs may be a useful adjuvant in the treatment of rapidly progressive osteosarcoma. epigenetics hsa-mir-431 Osteosarcoma 22957032 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Treatment with 4-phenylbutyrate increased acetylation of histones associated with 14q32 miRNAs, but interestingly, robust restoration of 14q32 miRNA expression, attenuation of cMYC expression, and induction of apoptosis required concomitant treatment with 5-Azacytidine, an inhibitor of DNA methylation. combination of these chromatin-modifying drugs may be a useful adjuvant in the treatment of rapidly progressive osteosarcoma. epigenetics hsa-mir-432 Osteosarcoma 22957032 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Treatment with 4-phenylbutyrate increased acetylation of histones associated with 14q32 miRNAs, but interestingly, robust restoration of 14q32 miRNA expression, attenuation of cMYC expression, and induction of apoptosis required concomitant treatment with 5-Azacytidine, an inhibitor of DNA methylation. combination of these chromatin-modifying drugs may be a useful adjuvant in the treatment of rapidly progressive osteosarcoma. epigenetics hsa-mir-570 Osteosarcoma 29795113 disease of cellular proliferation DOID:3347 D012516 259500 HP:0002669 Inhibition of LCMR1 and ATG12 by demethylation-activated miR-570-3p is involved in the anti-metastasis effects of metformin on human osteosarcoma. epigenetics hsa-mir-129-2 Ovarian Neoplasms 26519551 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 In summary, the obtained data indicate the involvement of methylation in the down-regulation of the studied coding and miRNA genes and suggest the involvement of miR-129-2 in the deregulation of RASSF1(A) via a direct interaction or/and mediators in common pathways (according to KEGG, Gene Ontology (FDR < 0.01), and GeneCards data) in the examined gynecological tumors. epigenetics hsa-mir-199b Ovarian Neoplasms 24659709 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Epigenetic silencing of microRNA-199b-5p is associated with acquired chemoresistance via activation of JAG1-Notch1 signaling in ovarian cancer. epigenetics hsa-mir-29b-1 Ovarian Neoplasms 23179556 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Anticancer role of MUC1 aptamer-miR-29b chimera in epithelial ovarian carcinoma cells through regulation of PTEN methylation epigenetics hsa-mir-29b-2 Ovarian Neoplasms 23179556 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Anticancer role of MUC1 aptamer-miR-29b chimera in epithelial ovarian carcinoma cells through regulation of PTEN methylation epigenetics hsa-mir-30d Ovarian Neoplasms 27141829 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 TET3 inhibits TGF-尾1-induced epithelial-mesenchymal transition by demethylating miR-30d precursor gene in ovarian cancer cells epigenetics hsa-mir-34a Ovarian Neoplasms 26879132 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 We demonstrated a clinical independent role of miR-34a in epithelial ovarian cancers. Moreover, we corroborated the correlation between miR-34a expression and its promoter methylation in a large set of ovarian cancers. The inverse association between miR-34a expression and grading, p53 mutation status and dualistic tumor type classification, together with its prognostic relevance may underline the tumor-suppressive character of miR-34a in ovarian cancer. epigenetics hsa-mir-34a Ovarian Neoplasms 21225432 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Ovarian Neoplasms 21225432 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Ovarian Neoplasms 21225432 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-9-1 Ovarian Neoplasms 26519551 endocrine system disease DOID:2394 C56 D010051 167000 HP:0100615 In summary, the obtained data indicate the involvement of methylation in the down-regulation of the studied coding and miRNA genes and suggest the involvement of miR-129-2 in the deregulation of RASSF1(A) via a direct interaction or/and mediators in common pathways (according to KEGG, Gene Ontology (FDR < 0.01), and GeneCards data) in the examined gynecological tumors. epigenetics hsa-mir-200 Ovarian Serous Cystadenocarcinoma 27746113 disease of cellular proliferation DOID:5746 D018284 DNA methylation-regulated microRNA pathways in ovarian serous cystadenocarcinoma: A meta-analysis. epigenetics hsa-mir-107 Pancreatic Neoplasms 19407485 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Epigenetic silencing of MicroRNA miR-107 regulates cyclin-dependent kinase 6 expression in pancreatic cancer. epigenetics hsa-mir-124-1 Pancreatic Neoplasms 23334332 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Methylation-mediated silencing of the miR-124 genes facilitates pancreatic cancer progression and metastasis by targeting Rac1 epigenetics hsa-mir-124-2 Pancreatic Neoplasms 23334332 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Methylation-mediated silencing of the miR-124 genes facilitates pancreatic cancer progression and metastasis by targeting Rac1 epigenetics hsa-mir-124-3 Pancreatic Neoplasms 23334332 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Methylation-mediated silencing of the miR-124 genes facilitates pancreatic cancer progression and metastasis by targeting Rac1 epigenetics hsa-mir-132 Pancreatic Neoplasms 21665894 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Downregulation of miR-132 by promoter methylation contributes to pancreatic cancer development. epigenetics hsa-mir-21 Pancreatic Neoplasms 24460329 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 MiR-21 upregulation induced by histone acetylation in the promoter zone is associated with chemoresistance to gemcitabine and enhanced malignant potential in pancreatic cancer cells. epigenetics hsa-mir-27a Pancreatic Neoplasms 20488920 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 microRNA-27a:Methyl 2-cyano-3,12-dioxooleana-1,9-dien-28-oate decreases specificity protein transcription factors and inhibits pancreatic tumor growth: role of microRNA-27a epigenetics hsa-mir-34a Pancreatic Neoplasms 21225432 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Pancreatic Neoplasms 21225432 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Pancreatic Neoplasms 21225432 disease of cellular proliferation DOID:1793 C25.0-.2 D010190 260350 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Pleural Mesothelioma 24168922 disease of cellular proliferation DOID:7474 C45.0 D054363 HP:0100002 Our digital MSP assay can quantify miR-34b/c methylation in serum-circulating DNA. The degree of miR-34b/c methylation in serum-circulating DNA is associated with MPM, suggesting that this approach might be useful for the establishment of a new detection system for MPM. epigenetics hsa-mir-34c Pleural Mesothelioma 24168922 disease of cellular proliferation DOID:7474 C45.0 D054363 HP:0100002 Our digital MSP assay can quantify miR-34b/c methylation in serum-circulating DNA. The degree of miR-34b/c methylation in serum-circulating DNA is associated with MPM, suggesting that this approach might be useful for the establishment of a new detection system for MPM. epigenetics hsa-mir-106b Polycystic Ovarian Syndrome 25243570 syndrome DOID:11612 E28.2 D011085 184700 Our data suggest that the expression of MCM7 and miR-93/25 is PCOSand IR related, whereas that of miR-106b is related to IR only. In 3T3-L1 adipocytes, neither hyperglycemia nor hyperinsulinemia altered the expression of miR-93 or miR-25, although increasing glucose levels down-regulated MCM7 and paradoxically increased that of miR-106b expression. The expression of the miR-25/93/106b family may be regulated through mechanisms distinct from its host gene, MCM7. Finally, our studies suggest potential epigenetic mechanisms for both IR and PCOS. epigenetics hsa-mir-25 Polycystic Ovarian Syndrome 25243570 syndrome DOID:11612 E28.2 D011085 184700 Our data suggest that the expression of MCM7 and miR-93/25 is PCOSand IR related, whereas that of miR-106b is related to IR only. In 3T3-L1 adipocytes, neither hyperglycemia nor hyperinsulinemia altered the expression of miR-93 or miR-25, although increasing glucose levels down-regulated MCM7 and paradoxically increased that of miR-106b expression. The expression of the miR-25/93/106b family may be regulated through mechanisms distinct from its host gene, MCM7. Finally, our studies suggest potential epigenetic mechanisms for both IR and PCOS. epigenetics hsa-mir-93 Polycystic Ovarian Syndrome 25243570 syndrome DOID:11612 E28.2 D011085 184700 Our data suggest that the expression of MCM7 and miR-93/25 is PCOSand IR related, whereas that of miR-106b is related to IR only. In 3T3-L1 adipocytes, neither hyperglycemia nor hyperinsulinemia altered the expression of miR-93 or miR-25, although increasing glucose levels down-regulated MCM7 and paradoxically increased that of miR-106b expression. The expression of the miR-25/93/106b family may be regulated through mechanisms distinct from its host gene, MCM7. Finally, our studies suggest potential epigenetic mechanisms for both IR and PCOS. epigenetics hsa-mir-34a Preeclampsia 29557690 cardiovascular system disease DOID:10591 O14 D011225 PS189800 HP:0100602 Hypomethylation of the miRNA-34a gene promoter is associated with Severe Preeclampsia epigenetics hsa-mir-124 Prostate Neoplasms 25860954 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Regulation and methylation of tumor suppressor miR-124 by androgen receptor in prostate cancer cells. epigenetics hsa-mir-1256 Prostate Neoplasms 22805767 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Epigenetic deregulation of miR-29a and miR-1256 by isoflavone contributes to the inhibition of prostate cancer cell growth and invasion. epigenetics hsa-mir-125b-2 Prostate Neoplasms 25728837 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Our work underlined the importance of histone demethylation and DNA oxidation/repairing machinery in androgen-dependent transcription. The present finds have implications for research into new druggable targets for prostate cancer relying on the cascade of AR activity regulation. epigenetics hsa-mir-1260b Prostate Neoplasms 24504368 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Our data suggest that genistein exerts its anti-tumour effect via downregulation of miR-1260b that targeted sRRP1 and Smad4 genes in prostate cancer cells. The expression of sFRP1 and Smad4 was also modulated by genistein via DNA methylation or histone modifications in PC cell lines. epigenetics hsa-mir-127 Prostate Neoplasms 17355635 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Human miR-127 is embedded in a CpG island and is silenced in several human cancers including bladder, prostate and colon cancer and has been suggested to play a role as a possible tumour suppressor gene. epigenetics hsa-mir-132 Prostate Neoplasms 22310291 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 DNA methylation silences miR-132 in prostate cancer. epigenetics hsa-mir-133b Prostate Neoplasms 25728837 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Our work underlined the importance of histone demethylation and DNA oxidation/repairing machinery in androgen-dependent transcription. The present finds have implications for research into new druggable targets for prostate cancer relying on the cascade of AR activity regulation. epigenetics hsa-mir-141 Prostate Neoplasms 27198154 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-200c and miR-141 are under epigenetic regulation in PCa cells. epigenetics hsa-mir-145 Prostate Neoplasms 25749421 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 A feedback regulation between miR-145 and DNA methyltransferase 3b in prostate cancer cell and their responses to irradiation. epigenetics hsa-mir-145 Prostate Neoplasms 21349819 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 this is the first report documenting that downregulation of miR-145 is through DNA methylation and p53 mutation pathways in prostate cancer. epigenetics hsa-mir-146a Prostate Neoplasms 24885368 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Up-regulating miR-146a expression via the hypomethylation of the miR-146a promoter by 5-Aza-CdR was correlated with delayed progression of castration-resistant prostate cancers. Moreover, site-specific DNA methylation may play an important role in miR-146a expression in androgen-dependent prostate cancer progression to androgen-independent prostate cancer and therefore provides a potentially useful biomarker for assessing drug efficacy in prostate cancer. epigenetics hsa-mir-148a Prostate Neoplasms 29596883 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-148a is silenced by DNA methylation and ectopic expression of miR-148a suppresses DNMT1 expression and induced apoptotic genes expression in hormone-refractory prostate cancer cells epigenetics hsa-mir-193b Prostate Neoplasms 20073067 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-193b:miR-193b is an epigenetically regulated putative tumor suppressor in prostate cancer epigenetics hsa-mir-193b Prostate Neoplasms 28143614 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 MiR-193b promoter methylation accurately detects prostate cancer in urine sediments and miR-34b/c or miR-129-2 promoter methylation define subsets of clinically aggressive tumors. epigenetics hsa-mir-196b Prostate Neoplasms 21255435 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 We find miR-205, miR-21, and miR-196b to be epigenetically repressed, and miR-615 epigenetically activated in prostate cancer cells. epigenetics hsa-mir-200c Prostate Neoplasms 27198154 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-200c and miR-141 are under epigenetic regulation in PCa cells. epigenetics hsa-mir-205 Prostate Neoplasms 21255435 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 We find miR-205, miR-21, and miR-196b to be epigenetically repressed, and miR-615 epigenetically activated in prostate cancer cells. epigenetics hsa-mir-205 Prostate Neoplasms 22869146 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Epigenetic-induced repression of microRNA-205 is associated with MED1 activation and a poorer prognosis in localized prostate cancer. epigenetics hsa-mir-21 Prostate Neoplasms 21255435 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 We find miR-205, miR-21, and miR-196b to be epigenetically repressed, and miR-615 epigenetically activated in prostate cancer cells. epigenetics hsa-mir-224 Prostate Neoplasms 24737792 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The GABRE-miR-452-miR-224 locus is downregulated and hypermethylated in prostate cancer and is a new promising epigenetic candidate biomarker for prostate cancer diagnosis and prognosis. Tumor-suppressive functions of the intronic miR-224 and miR-452 were demonstrated in two prostate cancer cell lines,suggesting that epigenetic silencing of GABRE/miR-452/miR-224 may be selected for in prostate cancer. epigenetics hsa-mir-23b Prostate Neoplasms 23074286 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miR-23b Represses Proto-oncogene Src Kinase and Functions as Methylation-Silenced Tumor Suppressor with Diagnostic and Prognostic Significance in Prostate Cancer epigenetics hsa-mir-29a Prostate Neoplasms 22805767 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Epigenetic deregulation of miR-29a and miR-1256 by isoflavone contributes to the inhibition of prostate cancer cell growth and invasion. epigenetics hsa-mir-31 Prostate Neoplasms 23233736 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Epigenetic repression of miR-31 disrupts androgen receptor homeostasis and contributes to prostate cancer progression epigenetics hsa-mir-34a Prostate Neoplasms 22347519 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Epigenetic silencing of miR-34a in human prostate cancer cells and tumor tissue specimens can be reversed by BR-DIM treatment. epigenetics hsa-mir-34b Prostate Neoplasms 23147995 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 miRNA-34b Inhibits Prostate Cancer through Demethylation, Active Chromatin Modifications, and AKT Pathways epigenetics hsa-mir-375 Prostate Neoplasms 24173286 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 Androgen receptor is negatively correlated with the methylation-mediated transcriptional repression of miR-375 in human prostate cancer cells. epigenetics hsa-mir-452 Prostate Neoplasms 24737792 disease of cellular proliferation DOID:10283 C51 D011471 176807 HP:0100787 The GABRE-miR-452-miR-224 locus is downregulated and hypermethylated in prostate cancer and is a new promising epigenetic candidate biomarker for prostate cancer diagnosis and prognosis. Tumor-suppressive functions of the intronic miR-224 and miR-452 were demonstrated in two prostate cancer cell lines,suggesting that epigenetic silencing of GABRE/miR-452/miR-224 may be selected for in prostate cancer. epigenetics hsa-mir-124 Pulmonary Hypertension 24385500 cardiovascular system disease DOID:6432 I27.20 D006976 PS178600 HP:0002092 Deacetylation of MicroRNA-124 in fibroblasts: role in pulmonary hypertension. epigenetics hsa-mir-203 Rhabdomyosarcoma 24247238 disease of cellular proliferation DOID:3247 M62.82 D012208 268220 HP:0002859 miR-203, a tumor suppressor frequently down-regulated by promoter hypermethylation in rhabdomyosarcoma. epigenetics hsa-mir-214 Rhabdomyosarcoma 24811402 disease of cellular proliferation DOID:3247 M62.82 D012208 268220 HP:0002859 MiR-214 and N-ras regulatory loop suppresses rhabdomyosarcoma cell growth and xenograft tumorigenesis. epigenetics hsa-mir-124a Rheumatoid Arthritis 24223605 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 The methylation status of miR-124a seen in this study concurs with that reported in tumor cells, indicating epigenetic dysregulation constituents, a mechanism in the development of rheumatoid arthritis. epigenetics hsa-mir-124a Rheumatoid Arthritis 27824863 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Demethylation of MicroRNA-124a Genes Attenuated Proliferation of Rheumatoid Arthritis Derived Fibroblast-Like Synoviocytes and Synthesis of Tumor Necrosis Factor-α. epigenetics hsa-mir-126 Rheumatoid Arthritis 26464634 musculoskeletal system disease DOID:7148 M06.9 D001172 180300 HP:0001370 Correlation between miR-126 expression and DNA hypomethylation of CD4+ T cells in rheumatoid arthritis patients. epigenetics hsa-mir-34a Sarcoma [unspecific] 21225432 disease of cellular proliferation DOID:1115 C49 D012509 HP:0100242 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Sarcoma [unspecific] 21225432 disease of cellular proliferation DOID:1115 C49 D012509 HP:0100242 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Sarcoma [unspecific] 21225432 disease of cellular proliferation DOID:1115 C49 D012509 HP:0100242 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Sarcomatoid Mesothelioma 26870271 disease of cellular proliferation DOID:4488 miR-34b/c was heavily methylated in 2/4 established MPM cell lines epigenetics hsa-mir-34c Sarcomatoid Mesothelioma 26870271 disease of cellular proliferation DOID:4488 miR-34b/c was heavily methylated in 2/4 established MPM cell lines epigenetics hsa-mir-148a Skin Neoplasms 26638007 disease of cellular proliferation DOID:4159 C44.90 D012878 HP:0008069 Taken together, the expression of miR-148a was regulated by DNA methylation and targeted by TGIF2.Its methylation may be a potential prognostic indicator in skin cancer. epigenetics hsa-mir-34b Soft Tissue Sarcoma 25773680 C49.9 D012509 HP:0030448 Hypermethylation of potential tumor suppressor miR-34b/c is correlated with late clinical stage in patients with soft tissue sarcomas. epigenetics hsa-mir-34c Soft Tissue Sarcoma 25773680 C49.9 D012509 HP:0030448 Hypermethylation of potential tumor suppressor miR-34b/c is correlated with late clinical stage in patients with soft tissue sarcomas. epigenetics hsa-mir-10b Squamous Cell Carcinoma 25312779 disease of cellular proliferation DOID:1749 D002294 Reduction of TIP30 in esophageal squamous cell carcinoma cells involves promoter methylation and microRNA-10b. epigenetics hsa-mir-297 Squamous Cell Carcinoma 24394434 disease of cellular proliferation DOID:1749 D002294 Phospho-ΔNp63α/microRNA network modulates epigenetic regulatory enzymes in squamous cell carcinomas. epigenetics hsa-mir-485 Squamous Cell Carcinoma 24394434 disease of cellular proliferation DOID:1749 D002294 Phospho-ΔNp63α/microRNA network modulates epigenetic regulatory enzymes in squamous cell carcinomas. epigenetics hsa-mir-92b Squamous Cell Carcinoma 24394434 disease of cellular proliferation DOID:1749 D002294 Phospho-ΔNp63α/microRNA network modulates epigenetic regulatory enzymes in squamous cell carcinomas. epigenetics hsa-mir-129-2 Squamous Cell Carcinoma, Esophageal 21547903 disease of cellular proliferation DOID:3748 C562729 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-145 Squamous Cell Carcinoma, Esophageal 26254350 disease of cellular proliferation DOID:3748 C562729 Suppressor microRNA-145 Is Epigenetically Regulated by Promoter Hypermethylation in Esophageal Squamous Cell Carcinoma. epigenetics hsa-mir-34a Squamous Cell Carcinoma, Esophageal 21547903 disease of cellular proliferation DOID:3748 C562729 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-34b Squamous Cell Carcinoma, Esophageal 21547903 disease of cellular proliferation DOID:3748 C562729 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-34c Squamous Cell Carcinoma, Esophageal 21547903 disease of cellular proliferation DOID:3748 C562729 The methylation ratio of miR-34a, miR-34b/c and miR-129-2 is 66.7%(36/54), 40.7%(22/54), and 96.3%(52/54) respectively in ESCC, which are significantly higher than that in corresponding non-tumor tissues(p<0.01). epigenetics hsa-mir-10b Squamous Cell Carcinoma, Head and Neck 27002147 disease of cellular proliferation DOID:5520 C76.0 C535575 DOT1L-associated epigenetic changes induced by HA play pivotal roles in miR-10 production leading to up-regulation of RhoGTPase and survival proteins. epigenetics hsa-mir-137 Squamous Cell Carcinoma, Head and Neck 21425146 disease of cellular proliferation DOID:5520 C76.0 C535575 MicroRNA-137 promoter methylation is associated with poorer overall survival in patients with squamous cell carcinoma of the head and neck. epigenetics hsa-mir-34a Squamous Cell Carcinoma, Laryngeal or Hypopharyngeal 27450916 disease of cellular proliferation DOID:2876 Our study revealed that miR-34a promoter hypermethylation was a risk factor for LSCC, played a critical role in the disease progression and metastasis, and could serve as a poor prognostic factor for LSCC. epigenetics hsa-mir-137 Squamous Cell Carcinoma, Oral 20197299 disease of cellular proliferation DOID:0050866 miR-137:MicroRNA-137 promoter methylation in oral rinses from patients with squamous cell carcinoma of the head and neck is associated with gender and body mass index epigenetics hsa-mir-137 Squamous Cell Carcinoma, Oral 23121285 disease of cellular proliferation DOID:0050866 MicroRNA-137 promoter methylation in oral lichen planus and oral squamous cell carcinoma epigenetics hsa-mir-9-1 Squamous Cell Carcinoma, Oral 22133638 disease of cellular proliferation DOID:0050866 Methylation of microRNA-9 is a specific and sensitive biomarker for oral and oropharyngeal squamous cell carcinomas. epigenetics hsa-mir-9-3 Squamous Cell Carcinoma, Oral 22133638 disease of cellular proliferation DOID:0050866 Methylation of microRNA-9 is a specific and sensitive biomarker for oral and oropharyngeal squamous cell carcinomas. epigenetics hsa-mir-126 Systemic Lupus Erythematosus 21165896 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 MicroRNA-126 regulates DNA methylation in CD4(+) T cells and contributes to systemic lupus erythematosus by targeting DNA methyltransferase 1. epigenetics hsa-mir-126 Systemic Lupus Erythematosus 21538319 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 MicroRNA-126 regulates DNA methylation in CD4+ T cells and contributes to systemic lupus erythematosus by targeting DNA methyltransferase 1. epigenetics hsa-mir-126 Systemic Lupus Erythematosus 23981988 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 The upregulation of miR-126 and its host gene EGFL7 expression in CD4+ T cells from SLE is associated with the hypomethylation of the EGFL7 promoter. epigenetics hsa-mir-142 Systemic Lupus Erythematosus 25661834 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 Data from this study suggest that MPA activates miR-142 and miR-146a expression through histone modification at the promoter region, which may partially explain the pharmacological mechanisms of MPA for SLE. epigenetics hsa-mir-146a Systemic Lupus Erythematosus 25661834 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 Data from this study suggest that MPA activates miR-142 and miR-146a expression through histone modification at the promoter region, which may partially explain the pharmacological mechanisms of MPA for SLE. epigenetics hsa-mir-29b-1 Systemic Lupus Erythematosus 23142053 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 MicroRNA-29b contributes to DNA hypomethylation of CD4+ T cells in systemic lupus erythematosus by indirectly targeting DNA methyltransferase 1 epigenetics hsa-mir-29b-2 Systemic Lupus Erythematosus 23142053 musculoskeletal system disease DOID:9074 M32.9 D008180 152700 HP:0002725 MicroRNA-29b contributes to DNA hypomethylation of CD4+ T cells in systemic lupus erythematosus by indirectly targeting DNA methyltransferase 1 epigenetics hsa-mir-371 Testicular Germ Cell Tumor 28199193 disease of cellular proliferation DOID:5557 C563236 273300 Epigenetic and risk factors of testicular germ cell tumors: a brief review. epigenetics hsa-mir-373 Testicular Germ Cell Tumor 28199193 disease of cellular proliferation DOID:5557 C563236 273300 Epigenetic and risk factors of testicular germ cell tumors: a brief review. epigenetics hsa-mir-199a Testicular Neoplasms 23959088 disease of cellular proliferation DOID:2998 D013736 273300 HP:0010788 microRNA-199a-3p, DNMT3A, and aberrant DNA methylation in testicular cancer. epigenetics hsa-mir-199a-1 Testicular Neoplasms 21383689 disease of cellular proliferation DOID:2998 D013736 273300 HP:0010788 PODXL is a downstream effector mediating the action of miR199a-5p. This report identifies DNA methylation, miR-199a dysregulation and PODXL as critical factors in tumor malignancy. epigenetics hsa-mir-199a-2 Testicular Neoplasms 21383689 disease of cellular proliferation DOID:2998 D013736 273300 HP:0010788 PODXL is a downstream effector mediating the action of miR199a-5p. This report identifies DNA methylation, miR-199a dysregulation and PODXL as critical factors in tumor malignancy. epigenetics hsa-mir-129-1 Thyroid Neoplasms 21946411 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Two HDACi, Trichostatin A and vorinostat, induced miR-129-5p overexpression, histone acetylation and cell death. In addition, miR-129-5p alone was sufficient to induce cell death and knockdown experiments showed that expression of this miRNA was required for HDACi-induced cell death. Moreover, miR-129-5p was also able to improve the anti-proliferative effects of other cancer drugs such as etoposide or HAMLET (human alpha lactalbumin made letal for tumor cells). Taken together, the data show that miR-129-5p is involved in the antitumor activity of HDACi and highlight that miRNA-driven cell death may be an efficient approach to cancer treatment. epigenetics hsa-mir-129-2 Thyroid Neoplasms 21946411 disease of cellular proliferation DOID:1781 C73 D013964 188550 HP:0100031 Two HDACi, Trichostatin A and vorinostat, induced miR-129-5p overexpression, histone acetylation and cell death. In addition, miR-129-5p alone was sufficient to induce cell death and knockdown experiments showed that expression of this miRNA was required for HDACi-induced cell death. Moreover, miR-129-5p was also able to improve the anti-proliferative effects of other cancer drugs such as etoposide or HAMLET (human alpha lactalbumin made letal for tumor cells). Taken together, the data show that miR-129-5p is involved in the antitumor activity of HDACi and highlight that miRNA-driven cell death may be an efficient approach to cancer treatment. epigenetics hsa-mir-1224 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-1227 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-1229 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-127 Urinary Bladder Cancer 17355635 urinary system disease DOID:11054 C67 D001749 109800 Human miR-127 is embedded in a CpG island and is silenced in several human cancers including bladder, prostate and colon cancer and has been suggested to play a role as a possible tumour suppressor gene. epigenetics hsa-mir-149 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-203 Urinary Bladder Cancer 21461574 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation of miR-124a and miR-203 in the precursor lesions compared to the control samples epigenetics hsa-mir-210 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-212 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-328 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-34a Urinary Bladder Cancer 21225432 urinary system disease DOID:11054 C67 D001749 109800 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34b Urinary Bladder Cancer 21225432 urinary system disease DOID:11054 C67 D001749 109800 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-34c Urinary Bladder Cancer 21225432 urinary system disease DOID:11054 C67 D001749 109800 Frequent concomitant inactivation of miR-34a and miR-34b/c by CpG methylation in colorectal, pancreatic, mammary, ovarian, urothelial, and renal cell carcinomas and soft tissue sarcomas. epigenetics hsa-mir-503 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-9-1 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-9-2 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-9-3 Urinary Bladder Cancer 21138856 urinary system disease DOID:11054 C67 D001749 109800 hypermethylation was more frequent and dense in CpG shores than islands epigenetics hsa-mir-143 Vascular Disease [unspecific] 26573388 cardiovascular system disease DOID:178 I72.9 D000783 Taken together, these findings suggest that DNMT3a is a direct target of miR-143, and that the upregulation of DNMT3 is responsible for the hypermethylation of miR-143 in Hcy-induced VSMC proliferation. epigenetics hsa-mir-206 Waldenstrom Macroglobulinemia 20519629 C88.0 D008258 153600 HP:0005508 miR-206:Waldenström macroglobulinemia (WM) cells present with increased expression of microRNA-206 (miRNA-206) and reduced expression of miRNA-9 epigenetics hsa-mir-9-1 Waldenstrom Macroglobulinemia 20519629 C88.0 D008258 153600 HP:0005508 miR-9:Waldenström macroglobulinemia (WM) cells present with increased expression of microRNA-206 (miRNA-206) and reduced expression of miRNA-9 epigenetics hsa-mir-9-2 Waldenstrom Macroglobulinemia 20519629 C88.0 D008258 153600 HP:0005508 miR-9:Waldenström macroglobulinemia (WM) cells present with increased expression of microRNA-206 (miRNA-206) and reduced expression of miRNA-9 epigenetics hsa-mir-34b Wilms Tumor 25625843 C64.2 D009396 PS194070 HP:0002667 Epigenetic analysis of sporadic and Lynch-associated ovarian cancers reveals histology-specific patterns of DNA methylation.