MiR-29c-3p Impairs the Adhesion of Endometrial Epithelial Cells via COL4A1/β-catenin in Endometriosis

Chengyuan Li, Jian Li, Li J, Li X, Xin Li, Geng L, Lan Geng, Zhang Q, Qiuju Zhang, Zhenhui Hou, Hou Z, Xi Xia, Xia X
American journal of reproductive immunology (New York, N.Y. : 1989) · 2026 · vol. 96(2) , pp. e70291 · doi:10.1111/aji.70291 · PMID:42579319 · PMC13460238 · W7202166576
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Abstract

OBJECTIVE: Defective endometrial receptivity is an indispensable cause of infertility in endometriosis, yet the post-transcriptional regulatory mechanisms underlying this impairment remain poorly understood. The goal of this research was to describe how miR-29c-3p and its target, COL4A1, regulate endometrial epithelial cell function and embryo adhesion. METHODS: Endometrial epithelial cells were obtained from 14 women (including 7 with endometriosis and 7 controls) undergoing in vitro fertilization (IVF). Expression levels of miR-29c-3p and COL4A1 were quantified. Gain- and loss-of-function tests were employed in Ishikawa cells to assess cell adhesion capabilities and delineate downstream signaling pathways implicated in implantation. RESULTS: Women with endometriosis had considerably higher levels of miR-29c-3p expression in their endometrial epithelium. Mechanistically, increased expression of miR-29c-3p suppressed COL4A1, downregulated E-cadherin, and impaired JAr spheroid attachment. Notably, COL4A1 knockdown recapitulated these phenotypes by encouraging epithelial-mesenchymal transition (EMT), thereby compromising adhesive capacity. CONCLUSION: Our findings identify the miR-29c-3p/COL4A1/β-catenin axis as a pivotal hub controlling endometrial epithelial adhesion. In patients with endometriosis, this axis could be a potential molecular candidate to enhance fertility outcomes and restore endometrial receptivity.

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MeSH descriptors

beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin Collagen Type IV Collagen Type IV Collagen Type IV Collagen Type IV Collagen Type IV Collagen Type IV Collagen Type IV Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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