Down regulation of MiR-93 contributes to endometriosis through targeting MMP3 and VEGFA.

Xuan Lv, Pei Chen, Wei Liu
American journal of cancer research · 2015 · vol. 5(5) , pp. 1706–17 · PMID:26175939 · W2395609882
article OA: green CC0 ⤵ 21 in-corpus citations
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Reduced miR-93 expression in endometriosis tissues was associated with increased MMP3 and VEGFA, which miR-93 directly targets to inhibit endometrial stromal cell proliferation and migration.

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Abstract

OBJECTIVE: This study aimed to explore the role of miRNAs in pathogenesis of endometriosis. METHODOLOGY: Endometrial samples from 57 females with endometriosis and 44 non-endometriotic controls were compared for the expression of a selected group of miRNAs. The regulatory function on downstream target was also explored. RESULTS: The expression of miR-93 and miR106a was significantly reduced in endometriotic samples compared to that in non-endometriotic samples. High levels of MMP3 and VEGFA were detected in more than 50% ectopic endometrium tissues. A negative association was found between the expression of miR-93 and the protein levels of MMP3 (Pearson correlation, r=-0.39, P=0.0025) or VEGFA (Pearson correlation, r=-0.37, P=0.0047) in samples from endometriosis patients. Mechanistically, miR-93 targeted MMP3 and VEGFA by directly binding to the 3'UTR of MMP3 and VEGFA mRNAs, and thereby inhibited the proliferation, migration and invasive capability of endometrial stromal cells (ESCs). CONCLUSION: The finding of this study suggests that deregulation of miR-93 contribute to endometriosis by up-regulation of MMP3 and VEGFA and thus provide potential therapeutic targets for the treatment of endometriosis.

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endometriosis

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