The crosstalk between oncogenic signaling and ferroptosis in cancer

• Published in: Critical reviews in oncology/hematology 2024-05, Vol.197, p.104349-104349, Article 104349
• Main Authors: Pang, Qianghu, Tang, Zhirou, Luo, Lianxiang
• Format: Article
• Language: English
• Subjects: ferroptosis; oncogenic signaling; oxidative stress; redox homeostasis; tumor
• ISSN: 1040-8428; 1879-0461
• DOI: 10.1016/j.critrevonc.2024.104349

Ferroptosis, a novel form of cell death regulation, was identified in 2012. It is characterized by unique features that differentiate it from other types of cell death, including necrosis, apoptosis, autophagy, and pyroptosis. Ferroptosis is defined by an abundance of iron ions and lipid peroxidation, resulting in alterations in subcellular structures, an elevation in reactive oxygen species (ROS), a reduction in glutathione (GSH) levels, and an augmentation in Fe (II) cytokines. Ferroptosis, a regulated process, is controlled by an intricate network of signaling pathways, where multiple stimuli can either enhance or hinder the process. This review primarily examines the defensive mechanisms of ferroptosis and its interaction with the tumor microenvironment. The analysis focuses on the pathways that involve AMPK, p53, NF2, mTOR, System Xc-, Wnt, Hippo, Nrf2, and cGAS-STING. The text discusses the possibilities of employing a combination therapy that targets several pathways for the treatment of cancer. It emphasizes the necessity for additional study in this field. [Display omitted] •Ferroptosis, an iron-dependent lipid peroxidative cell death mode, is closely related to tumors.•Tumor signaling pathways regulate ferroptosis.•Combined treatment of multiple signaling pathways contributes to the regulation of tumor ferroptosis.