Research progress on the key cuproptosis regulator FDX1 and its relevance to triple-negative breast cancer
- 1Department of Breast and Thyroid Surgery, the Affiliated Nanchong Central Hospital of North Sichuan Medical College , , ,
- 2The People’s Hospital of Tianfu New District , , ,
Abstract
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.
Related
- Biochanin A Induces Cuproptosis and Inhibits Lung Metastasis in triple-negative Breast Cancer
- Prognostic relevance of [18F]FDG PET/CT in triple-negative breast cancer: Results from the triple negative (TRINE)-PET trial
- Clinical research progress in hepatic cirrhosis
- Research Progress on Genotoxicity and Molecular Mechanisms of Environmental Endocrine Disruptors
- Research progress and practical applications of musculoskeletal ultrasound in military training injuries
BibTeX
@article{yuping2026research,
title = {{Research progress on the key cuproptosis regulator FDX1 and its relevance to triple-negative breast cancer}},
author = {Fan Yuping and Zeng Hongmiao and Yuan Songlin and Pu Chenchen and Zhu Kepeng},
journal = {Frontiers in molecular biosciences},
year = {2026},
month = oct,
doi = {10.3389/fmolb.2026.1985506},
url = {https://europepmc.org/article/PMC/PMC13728476},
note = {CC BY},
}
RIS
TY - JOUR
TI - Research progress on the key cuproptosis regulator FDX1 and its relevance to triple-negative breast cancer
AU - Fan Yuping
AU - Zeng Hongmiao
AU - Yuan Songlin
AU - Pu Chenchen
AU - Zhu Kepeng
PY - 2026
DA - 2026/10/20
JO - Frontiers in molecular biosciences
DO - 10.3389/fmolb.2026.1985506
UR - https://europepmc.org/article/PMC/PMC13728476
AB - 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.
SN - 2296-889X
ER -