ArticleOncology research2026
Inhibitory Effect of Progesterone on Breast Cancer Progression and Migration via the Regulation of Epithelial-Mesenchymal Transition.
Article in Oncology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
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Abstract
Objectives: Progesterone (P4) is believed to inhibit breast cancer growth, but its role in counteracting estrogen (E2)-driven progression remains unclear. This study aimed to investigate the inhibitory effect of P4 on E2-induced cell proliferation, migration, and invasion in Estrogen receptor (ER)+/progesterone receptor (PR)+ breast cancer cells by examining its regulatory role in the epithelial-mesenchymal transition (EMT). Methods: ER and PR-positive MCF-7 clonal variant (MCF-7 CV) breast cancer cells were treated with E2 and co-treated with various concentrations of P4. The effects on cell proliferation, migration, and invasion were assessed. The expression of key EMT markers (E-cadherin, N-cadherin, vimentin), transcription factors (Snail, Slug), and apoptosis-related genes (p53, B-cell lymphoma 2 [BCL-2], BCL2-associated X [BAX]) were analyzed. Results: P4 significantly inhibited E2-induced cell proliferation in a dose-dependent manner. In the presence of E2, P4 treatment reversed EMT characteristics by increasing E-cadherin while decreasing N-cadherin, vimentin, Snail, and Slug. Consequently, P4 inhibited E2-stimulated cell migration and invasion. Furthermore, P4 treatment promoted apoptosis by upregulating BAX and p53 and downregulating BCL-2. Conclusion: Progesterone can counteract estrogen-driven breast cancer progression in ER+/PR+ cells by inhibiting proliferation, reversing the EMT process, and inducing apoptosis. These findings provide mechanistic insight into the protective role of PR signaling in breast cancer.
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