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Ferroptosis in Cancer Cell Biology

Department of Translational Genomics, Medical Faculty, University of Cologne, Weyertal 155b, 50931 Cologne, Germany
Cologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Straße 26, 50931 Cologne, Germany
Department I of Internal Medicine, University Hospital of Cologne, Kerpener Straße 62, 50937 Cologne, Germany
Author to whom correspondence should be addressed.
Cancers 2020, 12(1), 164;
Received: 29 November 2019 / Revised: 7 January 2020 / Accepted: 7 January 2020 / Published: 9 January 2020
(This article belongs to the Special Issue Cell Death in Cancer)
A major hallmark of cancer is successful evasion of regulated forms of cell death. Ferroptosis is a recently discovered type of regulated necrosis which, unlike apoptosis or necroptosis, is independent of caspase activity and receptor-interacting protein 1 (RIPK1) kinase activity. Instead, ferroptotic cells die following iron-dependent lipid peroxidation, a process which is antagonised by glutathione peroxidase 4 (GPX4) and ferroptosis suppressor protein 1 (FSP1). Importantly, tumour cells escaping other forms of cell death have been suggested to maintain or acquire sensitivity to ferroptosis. Therefore, therapeutic exploitation of ferroptosis in cancer has received increasing attention. Here, we systematically review current literature on ferroptosis signalling, cross-signalling to cellular metabolism in cancer and a potential role for ferroptosis in tumour suppression and tumour immunology. By summarising current findings on cell biology relevant to ferroptosis in cancer, we aim to point out new conceptual avenues for utilising ferroptosis in systemic treatment approaches for cancer. View Full-Text
Keywords: ferroptosis; cancer; cell death; GPX4; inflammation ferroptosis; cancer; cell death; GPX4; inflammation
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Bebber, C.M.; Müller, F.; Prieto Clemente, L.; Weber, J.; von Karstedt, S. Ferroptosis in Cancer Cell Biology. Cancers 2020, 12, 164.

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