ArticleMolecules (Basel, Switzerland)2026
Diosmetin Modulates EMT-Associated Plasticity and Fibroblast-Activation Markers in Parallel Breast Cancer In Vitro Models.
Article in Molecules (Basel, Switzerland), 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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Abstract
Metastasis remains the leading cause of mortality in breast cancer and is closely linked to epithelial-mesenchymal transition (EMT) and tumor microenvironment (TME)-associated processes. Diosmetin (DT), the active metabolite of diosmin, a widely used venoactive drug, has emerged as a potential anticancer agent. Building on our previous findings demonstrating that DT enhances doxorubicin efficacy, this study investigated its effects on tumor cell plasticity and stromal activation-associated responses. EMT was induced in MCF-7 cells, while a stromal model was established by TGF-β-mediated activation of BJ fibroblasts toward a cancer-associated fibroblast (CAF)-like phenotype. Additionally, doxorubicin-induced senescence was generated in fibroblasts. Migration assays and quantitative real-time PCR were used to assess functional and transcriptional changes. EMT induction resulted in decreased
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