Novel insights on targeting ferroptosis in cancer therapy
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REVIEW
Open Access
Novel insights on targeting ferroptosis in cancer therapy Sipeng Zuo1,2†, Jie Yu1,2†, Hui Pan1,2* and Linna Lu1,2*
Abstract Ferroptosis belongs to a novel form of regulated cell death. It is characterized by iron dependence, destruction of intracellular redox balance and non-apoptosis. And cellular structure and molecules level changes also occur abnormally during ferroptosis. It has been proved that ferroptosis exist widespreadly in many diseases, such as heart disease, brain damage or alzheimer disease. At the same time, the role of ferroptosis in cancer cannot be underestimated. More and more indications have told that ferroptosis is becoming a powerful weapon against cancer. In addition, therapies rely on ferroptosis have been applied to the clinic. Therefore, it is necessary to understand this newly discovered form of cell death and its connection with cancer. This review summarizes the mechanism of ferroptosis, ferroptosis inducers based on different targets and inspection methods. At last, we analyzed the relationship between ferroptosis and malignancies, in order to provide a novel theory basis for cancer treatment. Keywords: Ferroptosis, Cancer, Therapy, Signaling pathway
Introduction Death is the ultimate destination of cells. The various forms of cell death are apoptosis, necrosis, pyroptosis, oncosis, and autophagy, and each form has its respective features [1]. A disruption of cell death as an approach to treat tumors has been pursued by numerous researchers. As a controlled cellular process, cell death is essential for maintaining tissue integrity and homeostasis, so a disruption of this process under human intervention may show clinical effects [2]. Ferroptosis, another form of cell death, has been observed many times. Cell death caused by insufficient cystine was discovered in the 1950s, and it could be rescued by the lipophilic antioxidant, tocopherol, a component of vitamin E [3, 4]. Subsequently, lipid peroxidation and reactive oxygen species (ROS) were found to be unfavorable for ferroptosis, and another key enzyme, * Correspondence: [email protected]; [email protected] † Sipeng Zuo and Jie Yu contributed equally to this work. 1 Department of Ophthalmology, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P. R. China Full list of author information is available at the end of the article
glutathione peroxidase 4 (GPX4), was isolated, purified, and confirmed to be involved in the cellular response to oxidative stress [5–7]. Interestingly, GPX4 overexpression has been reported to prevent oxidative stressinduced death in a mouse model [8]. The term ferroptosis, which referred to a novel type of iron-dependent programmed cell death, was introduced in 2012 [9]. Ferroptosis differs from other forms of cell death at biochemical, morphological, and genetic levels. Ferroptosis is characterized by its iron dependence, ability to disrupt the intracellular redox balance, and absence of apoptosis [10]. The differences between ferroptosis and apoptosis
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