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      Ferroptosis: challenges and opportunities for nanomaterials in cancer therapy

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          Abstract

          Ferroptosis, a completely new form of regulated cell death, is mainly caused by an imbalance between oxidative damage and reductive protection and has shown great anti-cancer potential. However, existing small-molecule ferroptosis inducers have various limitations, such as poor water solubility, drug resistance and low targeting ability, hindering their clinical applications. Nanotechnology provides new opportunities for ferroptosis-driven tumor therapy. Especially, stimuli-responsive nanomaterials stand out among others and have been widely researched because of their unique spatiotemporal control advantages. Therefore, it’s necessary to summarize the application of those stimuli-responsive nanomaterials in ferroptosis. Here, we describe the physiological feature of ferroptosis and illustrate the current challenges to induce ferroptosis for cancer therapy. Then, nanomaterials that induce ferroptosis are classified and elaborated according to the external and internal stimuli. Finally, the future perspectives in the field are proposed. We hope this review facilitates paving the way for the design of intelligent nano-ferroptosis inducers.

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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
                Qiaolin Liu
                Yuliang Zhao
                Huige Zhou
                Chunying Chen:
                ORCID: https://orcid.org/0000-0002-6027-0315
                Journal
                Journal ID (nlm-ta): Regen Biomater
                Journal ID (iso-abbrev): Regen Biomater
                Journal ID (publisher-id): rb
                Title: Regenerative Biomaterials
                Publisher: Oxford University Press
                ISSN (Print): 2056-3418
                ISSN (Electronic): 2056-3426
                Publication date Collection: 2023
                Publication date (Electronic): 20 January 2023
                Publication date PMC-release: 20 January 2023
                Volume: 10
                Electronic Location Identifier: rbad004
                Affiliations
                Henan Institutes of Advanced Technology, Zhengzhou University , Zhengzhou 450052, China
                CAS Key Laboratory for Biomedical Effects of Nanoparticles and Nanosafety & CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology , Beijing 100190, China
                CAS Key Laboratory for Biomedical Effects of Nanoparticles and Nanosafety & CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology , Beijing 100190, China
                University of Chinese Academy of Sciences , Beijing 100049, China
                Research Unit of Nanoscience and Technology, Chinese Academy of Medical Sciences , Beijing 100039, China
                The GBA National Institute for Nanotechnology Innovation , Guangzhou 510700, Guangdong, China
                CAS Key Laboratory for Biomedical Effects of Nanoparticles and Nanosafety & CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology , Beijing 100190, China
                University of Chinese Academy of Sciences , Beijing 100049, China
                Research Unit of Nanoscience and Technology, Chinese Academy of Medical Sciences , Beijing 100039, China
                CAS Key Laboratory for Biomedical Effects of Nanoparticles and Nanosafety & CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology , Beijing 100190, China
                University of Chinese Academy of Sciences , Beijing 100049, China
                Research Unit of Nanoscience and Technology, Chinese Academy of Medical Sciences , Beijing 100039, China
                The GBA National Institute for Nanotechnology Innovation , Guangzhou 510700, Guangdong, China
                Author notes
                Correspondence address. E-mail: chenchy@ 123456nanoctr.cn (C.C.); zhouhg@ 123456nanoctr.cn (H.Z.)
                Author information
                https://orcid.org/0000-0002-6027-0315
                Article
                Publisher ID: rbad004
                DOI: 10.1093/rb/rbad004
                PMC ID: 9926950
                PubMed ID: 36817975
                SO-VID: 149dd6f8-af10-4c2f-bbbd-83a81a5cbeb0
                Copyright © © The Author(s) 2023. Published by Oxford University Press.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 05 November 2022
                Date revision received : 11 December 2022
                Date accepted : 31 December 2022
                Date: 14 February 2023
                Page count
                Pages: 27
                Funding
                Funded by: Program for International S&T Cooperation Projects;
                Award ID: 2021YFE0112600
                Funded by: National Natural Science Foundation of China, DOI 10.13039/501100001809;
                Award ID: 32000983
                Award ID: 22027810
                Funded by: National Key R&D Program of China, DOI 10.13039/501100012166;
                Award ID: 2021YFA1200900
                Funded by: Strategic Priority Research Program of the Chinese Academy of Sciences;
                Award ID: XDB36000000
                Funded by: CAS Key Research Program for Frontier Sciences;
                Award ID: ZDBS-LY-SLH039
                Funded by: CAMS Innovation Fund for Medical Sciences;
                Award ID: CIFMS 2019-I2M-5-018
                Funded by: Research and Development Project in Key Areas of Guangdong Province;
                Award ID: 2019B090917011
                Categories
                Subject: Review
                Subject: AcademicSubjects/MED00010
                Subject: AcademicSubjects/SCI01410

                Keywords: ferroptosis,reactive oxygen species,stimuli-responsive nanomaterials,cancer therapy
                Data availability:
                Keywords: ferroptosis, reactive oxygen species, stimuli-responsive nanomaterials, cancer therapy

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