ArticleFrontiers in oncology2026
SIRT1 regulates glycolysis and angiogenesis of ovarian cancer through β-catenin/c-Myc/PKM2, and its mechanism in chemotherapy resistance.
Article in Frontiers in oncology, 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
Background: The purpose of this study is to explore the molecular mechanism of SIRT1 regulating chemotherapy resistance. Methods: Expression level of SIRT1 in ovarian cancer cell lines SKOV3, SKOV3/DDP (cisplatin-resistant cell line) and normal ovarian epithelial cell line IOSE80 was detected. Through the intervention of β-catenin agonist BML-284, the mechanism of SIRT1 regulating glycolysis and angiogenesis through β-catenin/c-myc/PKM2 pathway was discussed. Finally, the nude mice transplanted tumor model was constructed to verify the role of SIRT1 Results: The expression of SIRT1 increased in ovarian cancer cell line, especially in cisplatin-resistant cell line SKOV3/DDP. Knocking down SIRT1 can inhibit the proliferation, invasion and migration of ovarian cancer cells, promote cell apoptosis, and reduce the drug resistance of cells to cisplatin. SIRT1 enhances the malignant biological behavior of ovarian cancer cells by promoting glycolysis and angiogenesis. SIRT1 up-regulates the expression of key glycolytic enzymes and angiogenic factors by activating β-catenin/c-myc/PKM2 pathway. Conclusion: SIRT1 promotes glycolysis and angiogenesis of ovarian cancer cells by activating β-catenin/c-myc/PKM2 pathway, thus enhancing chemotherapy resistance. SIRT1 is expected to be a new target for ovarian cancer treatment.
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