Exploiting ferroptosis vulnerabilities in cancer

被引:19
|
作者
Nakamura, Toshitaka [1 ]
Conrad, Marcus [1 ]
机构
[1] Helmholtz Munich, Inst Metab & Cell Death, Mol Targets & Therapeut Ctr, Neuherberg, Germany
基金
欧洲研究理事会;
关键词
CELL-DEATH; T-CELLS; GLUTATHIONE SYNTHESIS; LIPID-PEROXIDATION; OXIDATIVE STRESS; GPX4; INHIBITION; SELENIUM; SUPPRESSOR; GROWTH;
D O I
10.1038/s41556-024-01425-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Ferroptosis is a distinct lipid peroxidation-dependent form of necrotic cell death. This process has been increasingly contemplated as a new target for cancer therapy because of an intrinsic or acquired ferroptosis vulnerability in difficult-to-treat cancers and tumour microenvironments. Here we review recent advances in our understanding of the molecular mechanisms that underlie ferroptosis and highlight available tools for the modulation of ferroptosis sensitivity in cancer cells and communication with immune cells within the tumour microenvironment. We further discuss how these new insights into ferroptosis-activating pathways can become new armouries in the fight against cancer. Ferroptosis is a form of cell death that is characterized by morphological abnormalities of mitochondria and the overwhelming peroxidation of phospholipids. Certain tumours are susceptible to ferroptosis, which could be exploited to treat cancers.
引用
收藏
页码:1407 / 1419
页数:13
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