The function and mechanism of ferroptosis in cancer
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REVIEW
The function and mechanism of ferroptosis in cancer Ying Wang1 · Zihao Wei1 · Keran Pan1 · Jing Li1 · Qianming Chen1 Accepted: 8 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
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. Keywords Ferroptosis · Cancer · p53 · Tumor-related ncRNA · TME · Ferroptosis-based cancer therapies
Introduction Cell death is inevitable in the process of life, whether resulting from physiological or pathological conditions, but cell death is also a complicated process. As the field continues to expand, the Nomenclature Committee on Cell Death (NCCD) has updated the classification of cell death pathways, which emphasizes mechanistic and other intrinsic aspects (as opposed to morphological, biochemical, and functional perspectives) of the cell death process [1]. Ferroptosis is a new form of regulated cell death (RCD) that differs from apoptosis, necrosis, pyroptosis and autophagy [1, 2]. To sustain the high demand for cell proliferation, cancer cells must undergo coordinated reprogramming of metabolic pathways that regulates the synthesis of amino acids, glycolysis, oxidative phosphorylation (OXPHOS), the tricarboxylic acid cycle (TCA), the pentose phosphate pathway (PPP), β-oxidation and glutaminolysis, which makes tumor cells * Jing Li [email protected] 1
State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, People’s Republic of China
heavily reliant on the intracellular antioxidant machinery [3, 4]. Coincidentally, ferroptosis can be activated by oxidative turbulence in the intracellular microenvironment, which is primarily controlled by glutathione peroxidase 4 (GPX4). Furthermore, amino acid metabolism, the TCA, the PPP, and glutaminolysis are associated with ferroptosis. Hence, we hypothesize that ferroptosis should play a potential and important role in cancer pro
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