ArticleIn vivo (Athens, Greece)
Metformin Inhibits the Estrogen-mediated Epithelial-Mesenchymal Transition of Ectopic Endometrial Stromal Cells in Endometriosis.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- SIRT1-mediated deacetylation of HMGB1 promotes the progression of endometriosis by regulating autophagy.Scientific reports · 2026Article
- Honokiol inhibits cell migration and invasion by blocking EMT via Snail/Slug axis in endometriosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- BDNF facilitates ectopic endometrial stromal cell growth, invasion, migration and glycolysis in endometriosis via upregulating GLUT1.CytoJournal · 2026Article
- Insights into the Molecular Mechanisms and Signaling Pathways of Epithelial to Mesenchymal Transition (EMT) in the Pathophysiology of Endometriosis.International journal of molecular sciences · 2025Review
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7 authors.
Funding
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Abstract
BACKGROUND/
aimEndometriosis 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
methodsWe 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.
resultsWe 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.
conclusionOur 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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