{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["16(12)"],"submitter":["Ma L"],"pubmed_abstract":["The detailed pathogenesis of endometriosis remains largely unclear despite decades of research. Recent studies have demonstrated that miRNAs plays an important role in endometriosis. The expression of miR-142-3p was decreased in ectopic endometrial tissues, while KLF9 and VEGFA expression levels were increased. Overexpression of miR-142-3p or knockdown of KLF9 significantly suppressed CRL-7566 cell proliferation and metastasis, induced cell apoptosis, and decreased both cell autophagy and vascularization. Additionally, KLF9 was confirmed to be a direct target of miR-142-3p and to directly bind to the promoter of the <i>VEGFA</i> gene, regulating its expression. Finally, intraperitoneal injection of miR-142-3p lentivirus significantly attenuated ectopic endometriotic lesions <i>in vivo</i>.miR-142-3p directly targeted KLF9, regulated VEGFA expression, and was protective against the growth of ectopic endometriotic lesions. Therefore, the miR-142-3p/KLF9/VEGFA signalling pathway may be a potential target in endometriosis treatment."],"journal":["RNA biology"],"pagination":["1733-1748"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6844572"],"repository":["biostudies-literature"],"pubmed_title":["MicroRNA-142-3p suppresses endometriosis by regulating KLF9-mediated autophagy <i>in vitro</i> and <i>in vivo</i>."],"pmcid":["PMC6844572"],"pubmed_authors":["Li W","Li Z","Ma L","Chen X","Ai J"],"additional_accession":[]},"is_claimable":false,"name":"MicroRNA-142-3p suppresses endometriosis by regulating KLF9-mediated autophagy <i>in vitro</i> and <i>in vivo</i>.","description":"The detailed pathogenesis of endometriosis remains largely unclear despite decades of research. Recent studies have demonstrated that miRNAs plays an important role in endometriosis. The expression of miR-142-3p was decreased in ectopic endometrial tissues, while KLF9 and VEGFA expression levels were increased. Overexpression of miR-142-3p or knockdown of KLF9 significantly suppressed CRL-7566 cell proliferation and metastasis, induced cell apoptosis, and decreased both cell autophagy and vascularization. Additionally, KLF9 was confirmed to be a direct target of miR-142-3p and to directly bind to the promoter of the <i>VEGFA</i> gene, regulating its expression. Finally, intraperitoneal injection of miR-142-3p lentivirus significantly attenuated ectopic endometriotic lesions <i>in vivo</i>.miR-142-3p directly targeted KLF9, regulated VEGFA expression, and was protective against the growth of ectopic endometriotic lesions. Therefore, the miR-142-3p/KLF9/VEGFA signalling pathway may be a potential target in endometriosis treatment.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Dec","modification":"2025-04-04T14:59:35.39Z","creation":"2020-08-29T07:19:57Z"},"accession":"S-EPMC6844572","cross_references":{"pubmed":["31425004"],"doi":["10.1080/15476286.2019.1657352"]}}