miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo

Zongwen Liang, Yijie Chen, Yuan Zhao, Chaoyi Xu, Anqi Zhang, Qiong Zhang, Danhan Wang, Jing He, Wenfeng Hua, Ping Duan
Stem cell research & therapy · 2017 · vol. 8(1) , pp. 251 · doi:10.1186/s13287-017-0706-z · PMID:29116025 · W2767225262
article OA: gold CC0 ⤵ 63 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

miR-200c suppresses endometriosis by targeting MALAT1, inhibiting proliferation and migration of endometrial stromal cells and decreasing endometriotic lesion growth in a rat model.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

The paper investigated how miR-200c affects endometriotic lesion biology by profiling miRNA expression in human endometrial tissue and testing the functional impact of miR-200c in primary human endometrial stromal cells (HESCs), with targets assessed using qPCR, proliferation and migration assays, and dual-luciferase reporter assays. Exogenous miR-200c overexpression inhibited HESC proliferation and migration, mechanistically linked to downregulation of the long noncoding RNA MALAT1, whereas miR-200c inhibition had opposite effects that were reversed by MALAT1 silencing; MALAT1 was reported to be negatively correlated with miR-200c in ectopic tissues. The study further showed that miR-200c mimic delivery in a rat model reduced growth of ectopic endometriotic lesions and modulated EMT marker proteins by decreasing ZEB1, ZEB2, and N-cadherin while increasing E-cadherin. A limitation explicitly implied by the design is reliance on in vitro HESC models and a single animal model rather than direct confirmation in broader human lesion contexts. This paper is centrally about endometriosis — it demonstrates that miR-200c suppresses endometriosis by targeting MALAT1 and influencing EMT-related factors.

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Abstract

BACKGROUND: Endometriosis is a common, benign, and estrogen-dependent disease characterized by pelvic pain and infertility. To date, the pathogenesis of endometriosis remains unclear. Recent studies have demonstrated that noncoding RNAs, including microRNAs and long noncoding RNAs, play important roles in the development of endometriosis. METHODS: Expression profiling of miRNAs in endometrial tissue was characterized using microarrays. The most differentially expressed miRNAs were confirmed using quantitative reverse transcriptase-polymerase chain reaction analysis in additional ectopic endometrial (n = 27) and normal endometrial (n = 12) tissues. For in-vitro functional studies, 5-ethynyl-2'-deoxyuridine incorporation assay, Transwell assay, and dual-luciferase reporter assay were used to measure the proliferation, migration, and luciferase activity of miR-200c and the predicted targets of miR-200c in primary endometrial stromal cells (HESCs) derived from human endometrial biopsies, respectively. For in-vivo therapeutic interventions, polymeric nanoparticles of polyethylenimine-polyethylene glycol-arginine-glycine-aspartic acid were used for delivery of miR-200c mimic and inhibitor to determine the therapeutic effect of miR-200c in a rat model of endometriosis. RESULTS: Exogenous overexpression of miR-200c inhibited the proliferation and migration of HESCs, which were mainly regulated by metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). In contrast, inhibition of miR-200c promoted the proliferation and migration of HESCs, while the simultaneous silencing of MALAT1 expression exerted the opposite effects. We demonstrated that expression of MALAT1 in ectopic endometrial specimens was negatively correlated with that of miR-200c and that MALAT1 knockdown increased the level of miR-200c in HESCs. Moreover, the transfection of endometrial stromal cells with the miR-200c mimic or MALAT1 siRNAs decreased the protein levels of mesenchymal markers ZEB1, ZEB2, and N-cadherin and increased the protein levels of the epithelial marker E-cadherin. Furthermore, using a rat endometriosis model, we showed that local delivery of the miR-200c mimic significantly inhibited the growth of ectopic endometriotic lesions. CONCLUSIONS: The MALAT1/miR-200c sponge may be a potential therapeutic target for endometriosis.

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Condition tags

mesh:D004715endometriosisinfertility

MeSH descriptors

Endometriosis Endometriosis MicroRNAs Nanoparticles RNA, Long Noncoding RNA, Long Noncoding Cell Line, Tumor Cell Proliferation Endometriosis Epithelial-Mesenchymal Transition Female Humans MicroRNAs MicroRNAs MicroRNAs Nanoparticles RNA, Long Noncoding Transfection

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