ArticleMedical oncology (Northwood, London, England)2026
Metformin sensitizes HepG2 liver cancer cells to doxorubicin through epithelial to mesenchymal transition and microRNA regulation.
Article in Medical oncology (Northwood, London, England), 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
Although therapeutic strategies have improved, liver cancer continues to impose a major global disease burden, largely due to its aggressive metastatic behavior and limited responsiveness to conventional chemotherapy. Metformin, a widely prescribed anti-diabetic drug, has shown emerging anti-tumor potential; however, its mechanisms, particularly in combination with chemotherapeutic agents, are not fully elucidated. This study explores the combined effects of metformin and the standard chemotherapeutic agent doxorubicin on the suppression of epithelial-to-mesenchymal transition (EMT), an essential driver of metastasis and chemoresistance, in HepG2 liver cancer cells. Low-dose combination treatment, optimized by SRB assay, markedly enhanced their antiproliferative activity compared with either drug alone. Consistently, wound-healing assays showed that the combined therapy more effectively inhibited HepG2 cell wound closure, suggesting a potential inhibitory effect on cell motility. Furthermore, the combined therapy altered EMT markers: upregulating epithelial markers (E-cadherin and Integrin-α5) while repressing mesenchymal markers Vimentin. These changes were accompanied by repression of key EMT-inducing transcription factors, including ZEB1, SNAIL1 and SNAIL2. Furthermore, qPCR analysis revealed that the combination significantly altered the expression of several EMT-associated miRNAs, including miR-215-5p, miR-122-5p, miR-429, miR-200c-3p, and miR-138-3p, with a strong upregulation of the miR-200 family, the classical EMT regulators. In conclusion, our findings show that metformin possesses anti-cancer effects that are significantly amplified when combined with doxorubicin. This combined treatment targeting the EMT pathway, offers a promising strategy to suppress metastasis and chemoresistance and improve therapeutic outcomes in liver cancer.
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