miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells

Chenfei Zhou, Chen-Fei Zhou, Min-juan Liu, Wei Wang, Sha Wu, Yuxin Huang, Yu-Xin Huang, Guo-Bin Chen, Li-Min Liu, Limin Liu, Dongxian Peng, Dong-Xian Peng, Xue-Feng Wang, Xuefeng Wang, Xuzi Cai, Xu-Zi Cai, Xiaoxuan Li, Xiao-Xuan Li, Wan-Qin Feng, Ying Ma
Stem cell research & therapy · 2019 · vol. 10(1) , pp. 287 · doi:10.1186/s13287-019-1388-5 · PMID:31547870 · W2976513195
article OA: gold CC0 ⤵ 25 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

miR-205-5p suppresses endometriosis progression by targeting ANGPT2 and inhibiting the ERK/AKT pathway in endometrial stromal cells, with expression levels correlating to disease severity.

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

This study examined microRNA profiles in ectopic endometrial (endometriosis) tissues versus normal endometrium, using miRNA microarray analysis followed by qRT-PCR validation, and then tested the functional role of the most downregulated miRNA, miR-205-5p. In primary ectopic endometrial stromal cells and a human endometrial-like xenograft model, miR-205-5p overexpression suppressed cell migration, invasion, and promoted apoptosis, while ANGPT2 was identified as a direct miR-205-5p target via luciferase reporter assays; rescuing/silencing ANGPT2 reversed/simulated miR-205-5p effects and implicated ERK/AKT pathway activation. The authors report correlations between miR-205-5p/ANGPT2 expression and endometriosis severity, but the clinical comparison used a small tissue microarray discovery set (n=3 per group). This paper is centrally about endometriosis — specifically how miR-205-5p inhibits endometriosis progression by targeting ANGPT2 and modulating ERK/AKT signaling.

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Abstract

BACKGROUND: miRNA expression profiles in ectopic endometrium (EC) serving as pathophysiologic genetic fingerprints contribute to determining endometriosis progression; however, the underlying molecular mechanisms remain unknown. METHODS: miRNA microarray analysis was used to determine the expression profiling of EC fresh tissues. qRT-PCR was performed to screen miR-205-5p expression in EC tissues. The roles of miR-205-5p and its candidate target gene, angiopoietin-2 (ANGPT2), in endometriosis progression were confirmed on the basis of both in vitro and in vivo systems. miR-205-5p and ANGPT2 expression were measured by in situ hybridization and immunochemistry, and their clinical significance was statistically analysed. RESULTS: miR-205-5p was screened as a novel suppressor of endometriosis through primary ectopic endometrial stromal cell migration, invasion, and apoptosis assay in vitro, along with endometrial-like xenograft growth and apoptosis in vivo. In addition, ANGPT2 was identified as a direct target of miR-205-5p through bioinformatic target prediction and luciferase reporter assay. Re-expression and knockdown of ANGPT2 could respectively rescue and simulate the effects induced by miR-205-5p. Importantly, the miR-205-5p-ANGPT2 axis was found to activate the ERK/AKT pathway in endometriosis. Finally, miR-205-5p and ANGPT2 expression were closely correlated with the endometriosis severity. CONCLUSION: The newly identified miR-205-5p-ANGPT2-AKT/ERK axis illustrates the molecular mechanism of endometriosis progression and may represent a novel diagnostic biomarker and therapeutic target for disease treatment.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Angiopoietin-2 Endometriosis Endometrium Mesenchymal Stem Cells MicroRNAs Angiopoietin-2 Angiopoietin-2 Animals Apoptosis Cells, Cultured Endometriosis Endometriosis Endometrium Endometrium Female Humans Mesenchymal Stem Cells Mice Mice, Nude MicroRNAs

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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.

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Cited by (25)

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