<p>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.</p>

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Advances in novel cell death mechanisms in breast cancer: intersecting perspectives on ferroptosis, cuproptosis, disulfidptosis, and pyroptosis

  • Zhengjun Jing,
  • Wenqin Huang,
  • Jun Mei,
  • Sudhanshu Bhushan,
  • Xinhong Wu,
  • Chengbiao Yan,
  • Hongmei Zheng,
  • Yalong Yang

摘要

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.