ArticleCancer medicine2026
Metronomic Capecitabine Triggers Ferroptosis in Hepatocellular Carcinoma Cells Through Inhibition of TYMS.
Article in Cancer medicine, 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
objectiveCapecitabine (CAP) is an orally administered prodrug of fluorouracil, predominantly utilized in the treatment of solid tumors. Triggering tumor ferroptosis is an important mechanism for the treatment of hepatocellular carcinoma (HCC). However, the potential of CAP to induce ferroptosis in HCC, along with the underlying mechanisms, remains unknown.
methodsIn this study, a subcutaneous HCC model was constructed using the syngeneic Hepa1-6 cell line in C57BL/6 mice, followed by treatment with metronomic CAP (mCAP). The anti-tumor effects of mCAP were evaluated by monitoring tumor volume, performing pathological staining, and evaluating tumor oxidative stress levels. In vitro, various thymidylate synthase (TYMS) inhibitors were used to treat both mouse and human HCC cell lines. Furthermore, TYMS-overexpressing plasmids were transfected into mouse and human HCC cell lines to directly investigate their impact on intracellular oxidative stress. Intracellular oxidative stress and ferroptosis-related markers were detected using flow cytometry, transmission electron microscopy, and Western blotting.
results5-FU, an active metabolite of CAP, as well as TYMS-specific inhibitors, suppressed the proliferation of Hepa1-6 and HepG2 cells. These treatments promoted p67
conclusionCAP targets TYMS to induce ferroptosis by activating NOX, thereby inhibiting HCC progression.
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