Please use this identifier to cite or link to this item: 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: http://ahro.austin.org.au/austinjspui/handle/1/16913
DOI: 10.1080/23723556.2017.1344757
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
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