ArticleAmerican journal of translational research2026
FBXO31-induced ABL2 ubiquitination increases cystine-glutamate antiporter-mediated ferroptosis and inhibits malignant progression in triple-negative breast cancer.
Article in American journal of translational research, 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
F-box only protein 31 (FBXO31) has been implicated in tumorigenesis and development across various human cancers. However, the role of FBXO31 in breast cancer progression remains poorly understood. In this study, we identified FBXO31 as a tumor suppressor in triple-negative breast cancer (TNBC), where it inhibited cell proliferation, migration, and invasion. Furthermore, FBXO31 promoted cystine-glutamate antiporter (xCT)-mediated ferroptosis in TNBC cells. Notably, overexpression of FBXO31 suppressed tumor growth in mice. Mechanistically, ABL-related gene (ABL2) was identified as a novel ubiquitin substrate of FBXO31. FBXO31 specifically interacted with ABL2 and promoted ABL2 ubiquitination and subsequent degradation through its F-box motif. Functionally, ABL2 acted as an oncogenic factor in TNBC cells by promoting cell proliferation, migration, and invasion, while inhibiting xCT-mediated ferroptosis. Rescue experiments showed that FBXO31 inhibited TNBC progression at least partly through down-regulating ABL2 expression. Collectively, our findings reveal a novel molecular mechanism for TNBC progression and provide a potential therapeutic strategy for its treatment.
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