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Life sciences · Journal article
Frontiers in Molecular Biosciences · October 20, 2026
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Cuproptosis, a recently identified form of programmed cell death driven by copper ion overload, occurs in a manner highly dependent on mitochondrial respiration and is orchestrated by the key reductase FDX1 (Ferredoxin 1). Triple-negative breast cancer (TNBC), the most aggressive subtype of breast cancer, lacks expression of the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2), rendering patients ineligible for endocrine therapy and anti-HER2 targeted treatments. Consequently, there is an urgent need to develop novel therapeutic strategies for this malignancy. The discovery of cuproptosis offers a fresh perspective for TNBC research: the prevalent metabolic reprogramming and hyperactive mitochondrial function characteristic of TNBC cells constitute an intrinsic vulnerability that may predispose them to cuproptosis induction. Emerging evidence indicates that low FDX1 expression may correlate with poor prognosis in TNBC, However, current evidence remains largely confined to mechanistic studies, bioinformatics analyses, and limited models; whether FDX1 expression correlates with prognosis in TNBC patients still awaits clinical translational validation.This review aims to systematically summarize the latest advances in research on the key cuproptosis regulator FDX1 and its relevance to TNBC, with the goal of providing directions for targeted therapeutic investigations in TNBC.