Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation, has become a key target in cancer therapy. SLC7A11, a cystine/glutamate antiporter, regulates ferroptosis by maintaining redox homeostasis through glutathione biosynthesis. In breast cancer, especially in aggressive subtypes like triple-negative breast cancer, SLC7A11 is frequently up-regulated and contributes to both ferroptosis resistance and tumor progression. This review examines SLC7A11's structure, regulation, and role in modulating ferroptotic sensitivity, its interactions with key oncogenic pathways such as PI3K/AKT/mTOR, and its involvement in immune modulation. Pharmacologic inhibition of SLC7A11, particularly in combination with immune checkpoint blockade or chemotherapy, shows therapeutic potential. Challenges remain, but future research should focus on biomarker-guided strategies to maximize ferroptosis-based therapies in clinical settings. SLC7A11 represents a promising therapeutic target for overcoming treatment resistance in breast cancer.
Fang et al. (Fri,) studied this question.
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