This review demonstrates the role of programmed cell death in breast cancer, highlighting novel pathways and therapy implications.
The advent of molecular classification has ushered breast cancer treatment into the era of precision medicine. Nevertheless, clinical management continues to face significant challenges posed by drug resistance and tumor heterogeneity. Recent advances have identified novel programmed cell death (PCD) mechanisms-including ferroptosis, cuproptosis, disulfidptosis, and pyroptosis-as critical regulators of breast cancer progression, therapeutic responsiveness, and immune microenvironment remodeling. This review systematically elucidates the mechanistic foundations of these PCD pathways and investigates their molecular regulatory networks within breast cancer pathogenesis. Furthermore, we evaluate current targeted intervention strategies and assess their clinical translation potential, ultimately providing a theoretical framework for pioneering therapeutic approaches.
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Jing et al. (2025) studied this question.
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