Abstract
Ferroptosis is a newly defined form of regulated cell death (RCD) characterized by iron overload, lipid reactive oxygen species (ROS) accumulation, and lipid peroxidation, which is different from necrosis, apoptosis, autophagy and other forms of RCD in morphology, biochemistry, function and gene expression. Increasing evidence has shown that ferroptosis is intimately associated with cancer initiation, progression, and suppression. In this review, we summarize the primary mechanisms and signal pathways relevant to ferroptosis and then discuss the potential roles of ferroptosis in cancer, including those related to p53, noncoding RNA (ncRNA), and the tumor microenvironment (TME), to demonstrate the associations between ferroptosis and cancer. Moreover, we list some ferroptosis-based cancer therapies, such as clinical drugs, nanomaterials, exosomes and gene technology, based on previous studies. Finally, we propose some development avenues, challenges, and opportunities for further research on ferroptosis.
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