Metformin Inhibits the Estrogen-mediated Epithelial-Mesenchymal Transition of Ectopic Endometrial Stromal Cells in Endometriosis

Yunkai Xie, Weimin Kong, Xiaoling Zhao, Dan Luo, Shuning Chen, HE ZHANG, H E Zhang, Yuliang Ran
In vivo (Athens, Greece) · 2023 · vol. 37(6) , pp. 2490–2497 · doi:10.21873/invivo.13356 · PMID:37905623 · PMC10621412 · W4388035099
article OA: diamond CC0 ⤵ 4 in-corpus citations
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Metformin inhibited estrogen-induced epithelial-mesenchymal transition, proliferation, migration, and invasion in ectopic endometrial stromal cells by downregulating EMT markers and β-catenin.

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Abstract

BACKGROUND/AIM: Endometriosis is an estrogen-dependent disease characterized by the ectopic implantation and growth of endometrial tissue outside the uterus. Endometrial stromal cells (ESCs) play a crucial role in the pathogenesis of endometriosis. Epithelial-mesenchymal transition (EMT) has recently been described in endometriosis and was induced by estrogen. Metformin has been shown to inhibit EMT in various diseases, but its role in endometriosis remains unclear. MATERIALS AND METHODS: We collected endometrial tissue samples from patients with endometriosis and healthy controls and isolated primary ESCs. We performed gene expression analysis using the Gene Expression Omnibus (GEO) dataset and validated the results by immunohistochemistry in tissue samples. We also assessed the effects of metformin on the proliferation, migration and invasion of ectopic ESCs (EESCs) by Cell Counting Kit-8 and Transwell migration and invasion assays, respectively. We analyzed the protein expression of EMT-related markers (N-cadherin, vimentin, twist, and snail) and β-catenin by Western blotting and immunohistochemistry. RESULTS: We found that vimentin was highly expressed in ectopic endometrial tissues compared to normal endometrial tissues. Metformin treatment inhibited the proliferation, migration and invasion of EESCs in a dose-dependent manner. Metformin treatment also downregulated the expression of EMT-related markers and reduced the expression and nuclear translocation of β-catenin in EESCs. CONCLUSION: Our results suggest that metformin inhibits estrogen-induced EMT and regulates the expression of β-catenin in EESCs. This study provides new insights into the potential therapeutic role of metformin in endometriosis.

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Condition tags

endometriosis

MeSH descriptors

beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin beta Catenin Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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