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Nakamura, T. ; Conrad, M.

Exploiting ferroptosis vulnerabilities in cancer.

Nat. Cell Biol., DOI: 10.1038/s41556-024-01425-8 (2024)
Verlagsversion DOI PMC
Closed
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Ferroptosis is a distinct lipid peroxidation-dependent form of necrotic cell death. This process has been increasingly contemplated as a new target for cancer therapy because of an intrinsic or acquired ferroptosis vulnerability in difficult-to-treat cancers and tumour microenvironments. Here we review recent advances in our understanding of the molecular mechanisms that underlie ferroptosis and highlight available tools for the modulation of ferroptosis sensitivity in cancer cells and communication with immune cells within the tumour microenvironment. We further discuss how these new insights into ferroptosis-activating pathways can become new armouries in the fight against cancer.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Cell-death; T-cells; Glutathione Synthesis; Lipid-peroxidation; Oxidative Stress; Gpx4; Inhibition; Selenium; Suppressor; Growth
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 1465-7392
e-ISSN 1476-4679
Zeitschrift Nature Cell Biology
Verlag Nature Publishing Group
Verlagsort Heidelberger Platz 3, Berlin, 14197, Germany
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Metabolism and Cell Death (MCD)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-506900-001
Förderungen European Research Council (ERC) under the European Union
EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activit
Deutsche Forschungsgemeinschaft (DFG)
CRC TRR 353
German Federal Ministry of Education and Research (BMBF) FERROPATH
DOI 10.1038/s41556-024-01425-8
WOS ID 001242786700002
Scopus ID 85195446941
PubMed ID 38858502
Erfassungsdatum 2024-06-12
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