ArticleTranslational andrology and urology2026
SESN2 promotes ferroptosis in bladder cancer by negatively regulating the NRF2/FSP1 signaling axis.
Article in Translational andrology and urology, 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: Bladder cancer (BLCA) shows intrinsic ferroptosis resistance. Sestrin2 (SESN2) regulates ferroptosis in other diseases, but its role in BLCA is unknown. In this study, we sought to determine whether SESN2 contributes to the intrinsic ferroptosis resistance of BLCA and to elucidate the underlying molecular mechanisms. Methods: SESN2 expression was measured in BLCA tissues, RT4 cells, T24 cells, and normal controls by quantitative real-time polymerase chain reaction, western blot, and immunofluorescence. Ferroptosis markers [glutathione (GSH), malondialdehyde (MDA), and Fe Results: SESN2 was downregulated in BLCA tissues and cells. BLCA displayed a ferroptosis-resistant phenotype (higher GSH, lower MDA and Fe Conclusions: SESN2 is downregulated in BLCA and promotes ferroptosis by negatively regulating the NRF2/FSP1 axis. This study identifies a novel role of SESN2 in BLCA ferroptosis and suggests targeting this pathway as a potential therapeutic strategy.
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