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Metabolic control of ferroptosis in cancer

Nature Cell Biology volume 20, pages 1104–1105 (2018)Cite this article

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Ferroptosis is a regulated non-apoptotic form of cell death and its functional role in tumorigenesis remains elusive. A study now shows that the tumour suppressor BAP1 enhances ferroptosis by modulating expression of the cystine transporter SLC7A11, leading to improved control of tumour growth.

Iron is an essential element for cell survival and its transport and storage are tightly regulated by iron-binding proteins1. However, free iron readily catalyses oxidative damage2. This catalytic process occurs through the formation of ferrous iron (Fe2+), which generates highly reactive free radicals that cause peroxidation of unsaturated fatty acids in membrane lipids leading to ferroptosis, a regulated form of cell death3,4. However, the function and regulation of ferroptosis in tumorigenesis remains unknown.

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Fig. 1: BAP1 enhances ferroptosis and suppresses tumorigenesis through SLC7A11.

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  1. Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK

    Michael P. Murphy

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  1. Michael P. Murphy
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Correspondence to Michael P. Murphy.

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Murphy, M.P. Metabolic control of ferroptosis in cancer. Nat Cell Biol 20, 1104–1105 (2018). https://doi.org/10.1038/s41556-018-0209-x

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  • DOI: https://doi.org/10.1038/s41556-018-0209-x

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