Ferroptosis is an iron- and lipid reactive oxygen species (ROS)-dependent form of programmed cell death that is distinct from other forms of regulatory cell death at the morphological, biological, and genetic levels. Emerging evidence suggests critical roles for ferroptosis in cell metabolism, the redox status, and various diseases, such as cancers, nervous system diseases, and ischemia-reperfusion injury, with ferroptosis-related proteins. Ferroptosis is inhibited in diverse cancer types and functions as a dynamic tumor suppressor in cancer development, indicating that the regulation of ferroptosis can be utilized as an interventional target for tumor treatment. Small molecules and nanomaterials that reprogram cancer cells to undergo ferroptosis are considered effective drugs for cancer therapy. Here, we systematically summarize the molecular basis of ferroptosis, the suppressive effect of ferroptosis on tumors, the effect of ferroptosis on cellular metabolism and the tumor microenvironment (TME), and ferroptosis-inducing agents for tumor therapeutics. An understanding of the latest progress in ferroptosis could provide references for proposing new potential targets for the treatment of cancers.

铁死亡是一种依赖铁和脂质活性氧 (ROS) 的程序性细胞死亡形式，在形态、生物学和遗传水平上不同于其他形式的调节性细胞死亡。新出现的证据表明，铁死亡在细胞代谢、氧化还原状态和各种疾病（如癌症、神经系统疾病和缺血再灌注损伤）中与铁死亡相关蛋白具有关键作用。铁死亡在多种癌症类型中受到抑制，并在癌症发展中作为动态肿瘤抑制因子发挥作用，表明铁死亡的调节可用作肿瘤治​​疗的介入靶点。重新编程癌细胞以经历铁死亡的小分子和纳米材料被认为是癌症治疗的有效药物。这里，我们系统地总结了铁死亡的分子基础、铁死亡对肿瘤的抑制作用、铁死亡对细胞代谢和肿瘤微环境（TME）的影响，以及用于肿瘤治疗的铁死亡诱导剂。了解铁死亡的最新进展可为提出治疗癌症的新潜在靶点提供参考。