<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16(12)</volume><submitter>Ma L</submitter><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 &lt;i>VEGFA&lt;/i> gene, regulating its expression. Finally, intraperitoneal injection of miR-142-3p lentivirus significantly attenuated ectopic endometriotic lesions &lt;i>in vivo&lt;/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.</pubmed_abstract><journal>RNA biology</journal><pagination>1733-1748</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6844572</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MicroRNA-142-3p suppresses endometriosis by regulating KLF9-mediated autophagy &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i>.</pubmed_title><pmcid>PMC6844572</pmcid><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Ma L</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Ai J</pubmed_authors></additional><is_claimable>false</is_claimable><name>MicroRNA-142-3p suppresses endometriosis by regulating KLF9-mediated autophagy &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i>.</name><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 &lt;i>VEGFA&lt;/i> gene, regulating its expression. Finally, intraperitoneal injection of miR-142-3p lentivirus significantly attenuated ectopic endometriotic lesions &lt;i>in vivo&lt;/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.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Dec</publication><modification>2025-04-04T14:59:35.39Z</modification><creation>2020-08-29T07:19:57Z</creation></dates><accession>S-EPMC6844572</accession><cross_references><pubmed>31425004</pubmed><doi>10.1080/15476286.2019.1657352</doi></cross_references></HashMap>