MicroRNA-142-3p suppresses endometriosis by regulating KLF9-mediated autophagy in vitro and in vivo

Lin Ma, Ma L, Zaiyi Li, Li Z, Li W, Weihao Li, Ai J, Jing Ai, Chen X, Xiaoxuan Chen
RNA biology · 2019 · vol. 16(12) , pp. 1733–1748 · doi:10.1080/15476286.2019.1657352 · PMID:31425004 · PMC6844572 · W2969522281
Lab / animal OA: bronze CC0 ⤵ 27 in-corpus citations
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This study found that microRNA-142-3p suppresses endometriosis by targeting KLF9 and regulating VEGFA expression, thereby inhibiting cell proliferation, metastasis, and autophagy both *in vitro* and *in vivo*.

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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 VEGFA gene, regulating its expression. Finally, intraperitoneal injection of miR-142-3p lentivirus significantly attenuated ectopic endometriotic lesions in vivo.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.

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Condition tags

endometriosis

MeSH descriptors

Autophagy Choristoma Endometriosis Kruppel-Like Transcription Factors MicroRNAs Neovascularization, Pathologic Vascular Endothelial Growth Factor A Animals Animals Apoptosis Apoptosis Apoptosis Autophagy Autophagy Base Pairing Base Pairing Base Sequence Base Sequence Cell Line Cell Line

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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Cited by (28)

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