依赖铁元素的脂质过氧化导致铁•诱导的非程序性细胞死亡（ferroptosis）。ferroptosis的形成关键步骤包括亚铁离子（Fe2+）的积累和脂质过氧化，这些都受到谷胱甘肽过氧化物酶4（GPX4）的调控。近十年来，许多研究已经证明了其在抑制癌症扩散中的重要作用。上皮间质转化（EMT）是上皮细胞获得间质特征的过程。EMT与癌变、侵袭性、转移性和治疗抵抗力等癌症特征相关。EMT受到一系列内外信号的控制，使细胞表型从上皮样转变为间质样。研究表明，间质型癌细胞更易出现ferroptosis，相比之下上皮型细胞则较少。当耐药癌细胞经历EMT时，它们更容易被诱导ferroptosis的药物杀灭。因此，了解ferroptosis与EMT之间的相互作用有助于确定新的癌症治疗靶点。对ferroptosis的调控、EMT在癌症治疗中的潜在应用以及与肿瘤有关的信号通路之间的关系进行了深入探讨。癌症的侵袭、转移和炎症中均包含ferroptosis和EMT。本综述的目标是为未来的研究提供建议，并为ferroptosis和EMT在临床实践中的应用提供实用指导。© 2023. 作者。

Iron-dependent lipid peroxidation causes ferroptosis, a form of regulated cell death. Crucial steps in the formation of ferroptosis include the accumulation of ferrous ions (Fe2+) and lipid peroxidation, of which are controlled by glutathione peroxidase 4 (GPX4). Its crucial role in stopping the spread of cancer has been shown by numerous studies undertaken in the last ten years. Epithelial-mesenchymal transition (EMT) is the process by which epithelial cells acquire mesenchymal characteristics. EMT is connected to carcinogenesis, invasiveness, metastasis, and therapeutic resistance in cancer. It is controlled by a range of internal and external signals and changes the phenotype from epithelial to mesenchymal like. Studies have shown that mesenchymal cancer cells tend to be more ferroptotic than their epithelial counterparts. Drug-resistant cancer cells are more easily killed by inducers of ferroptosis when they undergo EMT. Therefore, understanding the interaction between ferroptosis and EMT will help identify novel cancer treatment targets. In-depth discussion is given to the regulation of ferroptosis, the potential application of EMT in the treatment of cancer, and the relationships between ferroptosis, EMT, and signaling pathways associated with tumors. Invasion, metastasis, and inflammation in cancer all include ferroptosis and EMT. The goal of this review is to provide suggestions for future research and practical guidance for applying ferroptosis and EMT in clinical practice.© 2023. The Author(s).