Metformin regulates stromal-epithelial cells communication via Wnt2/β-catenin signaling in endometriosis

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Metformin regulates stromal-epithelial cell communication in endometriosis by modulating Wnt2/β-catenin signaling.

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Abstract

In previous studies, we found that endometriotic stromal cells lose the ability to regulate cell survival signaling in endometriotic epithelial cells. Here, we invested the effect of Metformin on the stromal-epithelial cells crosstalk in endometriosis and explored the pathway that might be involved. We found that ectopic endometriotic stromal cells (ESC) expressed and secreted higher Wnt2 protein compared with normal endometrial stromal cells (NSC). Conditioned medium (CM) from ESC supplemented with Wnt2 antibody significantly inhibited the growth of normal endometrial epithelial cells (NEC), while CM from ESC per se showed no significant effect on the growth of NEC. Metformin decreased the expression and secretion of Wnt2 in ESC. CM from Metformin-pretreated ESC significantly inhibited the growth of NEC. In conclusion, Wnt2/β-catenin signaling was involved in stromal-epithelial cells interaction in endometriosis. Metformin might regulate the stroma-epithelium communication via Wnt2-mediated signaling in endometriosis.

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Condition tags

endometriosis

MeSH descriptors

beta Catenin Cell Communication Endometriosis Epithelial Cells Metformin Wnt2 Protein Wnt Signaling Pathway Adult Adult beta Catenin beta Catenin Cell Communication Cell Communication Endometriosis Endometriosis Endometriosis Epithelial Cells Epithelial Cells Epithelial Cells Female

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (20)

Cited by (17)

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