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      Ferroptosis in tumor immunity and therapy

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          Abstract

          Ferroptosis is a type of regulated cell death (RCD), and it plays an important role in the occurrence of diseases, especially the development of tumors. Ferroptosis of tumor cells affects the antitumor immunity and the immune response to treatment to varying degrees. Ferroptosis also plays a key role in immune cells. This review outlines the mechanism of the immune‐related effects of ferroptosis pathways in tumor progression and treatment, and it discusses potential methods for improving antitumor immunity and enhancing the efficacy of current cancer treatments by targeting ferroptosis.

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          Ferroptosis: an iron-dependent form of nonapoptotic cell death.

          Scott J. Dixon, Kathryn Lemberg, Michael Lamprecht … (2012)
          Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

            Suzy Torti, Donna D. Zhang, K.A. Woerpel … (2019)
            Ferroptosis is a form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides to lethal levels. Emerging evidence suggests that ferroptosis represents an ancient vulnerability caused by the incorporation of polyunsaturated fatty acids into cellular membranes, and cells have developed complex systems that exploit and defend against this vulnerability in different contexts. The sensitivity to ferroptosis is tightly linked to numerous biological processes, including amino acid, iron, and polyunsaturated fatty acid metabolism, and the biosynthesis of glutathione, phospholipids, NADPH, and coenzyme Q10. Ferroptosis has been implicated in the pathological cell death associated with degenerative diseases (i.e., Alzheimer's, Huntington's, and Parkinson's diseases), carcinogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in mammals and is also implicated in heat stress in plants. Ferroptosis may also have a tumor-suppressor function that could be harnessed for cancer therapy. This Primer reviews the mechanisms underlying ferroptosis, highlights connections to other areas of biology and medicine, and recommends tools and guidelines for studying this emerging form of regulated cell death.
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              Regulation of ferroptotic cancer cell death by GPX4.

              Wan Seok Yang, Rohitha SriRamaratnam, Matthew E Welsch … (2014)
              Ferroptosis is a form of nonapoptotic cell death for which key regulators remain unknown. We sought a common mediator for the lethality of 12 ferroptosis-inducing small molecules. We used targeted metabolomic profiling to discover that depletion of glutathione causes inactivation of glutathione peroxidases (GPXs) in response to one class of compounds and a chemoproteomics strategy to discover that GPX4 is directly inhibited by a second class of compounds. GPX4 overexpression and knockdown modulated the lethality of 12 ferroptosis inducers, but not of 11 compounds with other lethal mechanisms. In addition, two representative ferroptosis inducers prevented tumor growth in xenograft mouse tumor models. Sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPX4-regulated ferroptosis. Thus, GPX4 is an essential regulator of ferroptotic cancer cell death. Copyright © 2014 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Jingying Li: jingyingli@ncu.edu.cn
                Kai Huang: kaihuang@ncu.edu.cn
                Xingen Zhu: ndefy89006@ncu.edu.cn
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J Cell Mol Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 01 November 2022
                Publication date (Print): November 2022
                Volume: 26
                Issue: 22 ( doiID: 10.1111/jcmm.v26.22 )
                Pages: 5565-5579
                Affiliations
                [ 1 ] Department of Neurosurgery The Second Affiliated Hospital of Nanchang University Nanchang China
                [ 2 ] Institute of Neuroscience, Nanchang University Nanchang China
                [ 3 ] Jiangxi Key Laboratory of Neurological Tumors and Cerebrovascular Diseases Nanchang China
                [ 4 ] College of Queen Mary Nanchang University Nanchang China
                [ 5 ] Department of Comprehensive Intensive Care Unit Second Affiliated Hospital of Nanchang University Nanchang China
                Author notes
                [*] [* ] Correspondence

                Xingen Zhu and Kai Huang, Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.

                Emails: ndefy89006@ 123456ncu.edu.cn ; kaihuang@ 123456ncu.edu.cn

                Jingying Li, Department of Comprehensive Intensive Care Unit, Second Affiliated Hospital of Nanchang University, Nanchang, China.

                Email: jingyingli@ 123456ncu.edu.cn

                Author information
                https://orcid.org/0000-0003-2024-1146
                Article
                Publisher ID: JCMM17529 Other ID: JCMM-03-2022-054.R2
                DOI: 10.1111/jcmm.17529
                PMC ID: 9667519
                PubMed ID: 36317423
                SO-VID: 37426309-bf72-4f01-b6b3-1526decf4187
                Copyright © © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date revision received : 11 July 2022
                Date received : 21 March 2022
                Date accepted : 14 July 2022
                Page count
                Figures: 3, Tables: 1, Pages: 15, Words: 11289
                Funding
                Funded by: Jiangxi Province Department of Education Science and technology research project
                Award ID: GJJ210177
                Funded by: Jiangxi Training Program for academic and technical leaders of major disciplines ‐‐ Young talents program
                Award ID: 20212BCJ23023
                Funded by: Key Research and Development projects in Jiangxi
                Award ID: 20212BBG73021
                Funded by: National Natural Science Foundation of China , doi 10.13039/501100001809;
                Award ID: 81760445
                Award ID: 81760446
                Award ID: 81960456
                Award ID: 82002660
                Categories
                Subject: Review
                Subject: Review
                Custom metadata
                source-schema-version-number 2.0
                cover-date November 2022
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.1 mode:remove_FC converted:16.11.2022

                ScienceOpen disciplines: Molecular medicine
                Keywords: ferroptosis,immune,lipid peroxidation,therapy,tumor microenvironment
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: ferroptosis, immune, lipid peroxidation, therapy, tumor microenvironment

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