ArticleCell death and differentiation2026
FDX1-short proteoform induces caspase-independent cell death in tumor cells.
Article in Cell death and differentiation, 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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15 authors.
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Abstract
Cell death is a crucial process for the maintenance of physiological functions in organisms. In recent years, cuproptosis, a novel form of cell death induced by copper overload in mitochondria, has emerged as a critical regulatory mechanism. Ferredoxin 1 (FDX1), a key electron transfer protein in this pathway, is essential for copper metabolism and the regulation of cuproptosis. In this study, we characterized a natural short proteoform of FDX1, FDX1-Short Proteoform (FDX1-SP). Lacking the canonical N-terminal mitochondrial targeting sequence, FDX1-SP is widely distributed throughout the cell, with a pronounced propensity for nuclear accumulation. The accumulation of FDX1-SP protein triggers cleavage and degradation of tumor cell DNA. This disrupts nuclear membrane integrity and induces cell death in a caspase-independent manner. FDX1-SP preferentially damages highly accessible chromatin regions in tumor cells, thereby inducing tumor cell death. Based on these findings, we developed an FDX1-SP mRNA therapeutic, which exhibited significant DNA damage and anti-tumor effects in patient-derived xenograft (PDX) models. Our research uncovers the mechanism of death mediated by FDX1-SP, providing new directions for tumor therapy.
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Registered trials
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