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

Lin Ma, Zaiyi Li, Weihao Li, Jing Ai, Xiaoxuan Chen
RNA biology · 2019 · vol. 16(12) , pp. 1733–1748 · doi:10.1080/15476286.2019.1657352 · PMID:31425004 · PMC6844572 · W2969522281
article OA: bronze CC0 ⤵ 27 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

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 Apoptosis Apoptosis Autophagy Base Pairing Base Sequence Cell Line Cell Proliferation Choristoma Choristoma Choristoma Disease Models, Animal Endometriosis

Citation neighborhood

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. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (56)

Cited by (27)

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