Targeting Ferroptosis in prostate cancers with SPOP and CHD1 defects
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SPOP mutations and CHD1 deletion define distinct prostate cancer subtypes with differential ferroptosis susceptibility. SPOP mutations enhance, while CHD1 deletion impairs, GPX4 inhibitor efficacy through opposing regulation of the MYC–ACSL4 axis. Cholesterol-lowering agents restore ACSL4 expression, re-sensitizing SPOP/CHD1 co-deficient tumors to ferroptosis. These findings establish biomarker-driven combinatorial strategies for ferroptosis-based therapy in advanced prostate cancer.
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Zenodo创建时间：
2026-04-23
