坏死性下垂
免疫系统
程序性细胞死亡
癌细胞
免疫原性细胞死亡
生物
自噬
肿瘤微环境
癌症研究
裂谷1
免疫耐受
细胞生物学
细胞凋亡
GPX4
癌症
免疫学
氧化应激
免疫疗法
生物化学
遗传学
谷胱甘肽过氧化物酶
过氧化氢酶
作者
Qin Dang,Ziqi Sun,Yang Wang,Libo Wang,Zaoqu Liu,Xinwei Han
标识
DOI:10.1038/s41419-022-05384-6
摘要
Abstract The term ferroptosis was put forward in 2012 and has been researched exponentially over the past few years. Ferroptosis is an unconventional pattern of iron-dependent programmed cell death, which belongs to a type of necrosis and is distinguished from apoptosis and autophagy. Actuated by iron-dependent phospholipid peroxidation, ferroptosis is modulated by various cellular metabolic and signaling pathways, including amino acid, lipid, iron, and mitochondrial metabolism. Notably, ferroptosis is associated with numerous diseases and plays a double-edged sword role. Particularly, metastasis-prone or highly-mutated tumor cells are sensitive to ferroptosis. Hence, inducing or prohibiting ferroptosis in tumor cells has vastly promising potential in treating drug-resistant cancers. Immunotolerant cancer cells are not sensitive to the traditional cell death pathway such as apoptosis and necroptosis, while ferroptosis plays a crucial role in mediating tumor and immune cells to antagonize immune tolerance, which has broad prospects in the clinical setting. Herein, we summarized the mechanisms and delineated the regulatory network of ferroptosis, emphasized its dual role in mediating immune tolerance, proposed its significant clinical benefits in the tumor immune microenvironment, and ultimately presented some provocative doubts. This review aims to provide practical guidelines and research directions for the clinical practice of ferroptosis in treating immune-resistant tumors.
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