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乳腺癌新型细胞死亡机制的研究进展:铁死亡、铜死亡、二硫死亡和焦亡的交叉视角

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

作者信息

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

机构信息

Department of Thyroid and Breast Surgery, Gong'an County People's Hospital, Gong'an County, 434300, Hubei Province, China.

Department of Breast Surgery, Breast Cancer Center, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, National Key Clinical Specialty Construction Discipline, Hubei Provincial Clinical Research Center for Breast Cancer, Wuhan Clinical Research Center for Breast Cancer, No.116 Zhuo Daoquan South Road, Wuhan, 430079, Hubei, China.

出版信息

Mol Cancer. 2025 Aug 27;24(1):224. doi: 10.1186/s12943-025-02445-0.

Abstract

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.

摘要

分子分类的出现将乳腺癌治疗带入了精准医学时代。然而,临床管理仍面临着耐药性和肿瘤异质性带来的重大挑战。最近的进展已经确定了新的程序性细胞死亡(PCD)机制,包括铁死亡、铜死亡、二硫死亡和焦亡,它们是乳腺癌进展、治疗反应性和免疫微环境重塑的关键调节因子。本综述系统地阐明了这些PCD途径的机制基础,并研究了它们在乳腺癌发病机制中的分子调控网络。此外,我们评估了当前的靶向干预策略,并评估了它们的临床转化潜力,最终为开拓性治疗方法提供了一个理论框架。

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