Inhibiting system x(C)(-) and glutathione biosynthesis - a potential Achilles' heel in mutant-p53 cancers
AuthorClemons, NJ; Liu, DS; Duong, CP; Phillips, WA
Source TitleMolecular & cellular oncology
PublisherTAYLOR & FRANCIS INC
AffiliationSir Peter MacCallum Department of Oncology
Surgery (St Vincent's)
Document TypeJournal Article
CitationsClemons, N. J., Liu, D. S., Duong, C. P. & Phillips, W. A. (2017). Inhibiting system x(C)(-) and glutathione biosynthesis - a potential Achilles' heel in mutant-p53 cancers. MOLECULAR & CELLULAR ONCOLOGY, 4 (5), https://doi.org/10.1080/23723556.2017.1344757.
Access StatusOpen Access
NHMRC Grant codeNHMRC/1120293
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.
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