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https://ahro.austin.org.au/austinjspui/handle/1/16913| Title: | Inhibiting system xC− and glutathione biosynthesis – a potential Achilles' heel in mutant-p53 cancers | Austin Authors: | Clemons, Nicholas J;Liu, David S;Duong, Cuong P;Phillips, Wayne A | Affiliation: | Division of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Victoria, Australia Division of Cancer Surgery, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia Department of Surgery, Austin Health, Heidelberg, Victoria, Australia Department of Surgery (St Vincent's Hospital), The University of Melbourne, Parkville, Victoria, Australia |
Issue Date: | 5-Jul-2017 | Publication information: | Molecular & Cellular Oncology 2017; 4(5): e1344757 | Abstract: | Effective therapeutic strategies to target mutant tumor protein p53 (TP53, best known as p53) cancers remain an unmet medical need. We found that mutant p53 impairs the function of nuclear factor (erythroid-derived 2)-like 2 (NFE2L2, commonly known as NRF2), suppresses solute carrier family 7 member 11 (SLC7A11) expression, and diminishes cellular glutamate/cystine exchange. This decreases glutathione biosynthesis, resulting in redox imbalance. Mutant p53 tumors are thus inherently susceptible to further perturbations of the SLC7A11/glutathione axis. | URI: | https://ahro.austin.org.au/austinjspui/handle/1/16913 | DOI: | 10.1080/23723556.2017.1344757 | Journal: | Molecular & Cellular Oncology | PubMed URL: | https://pubmed.ncbi.nlm.nih.gov/29057306 | Type: | Journal Article | Subjects: | APR-246 NFE2L2 NRF2 PRIMA-1met SLC7A11 glutathione (GSH) p53 reactive oxygen species (ROS) system xC− xCT |
| Appears in Collections: | Journal articles |
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