Inhibiting system x(C)(-) and glutathione biosynthesis - a potential Achilles' heel in mutant-p53 cancers

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Author
Clemons, NJ; Liu, DS; Duong, CP; Phillips, WADate
2017-01-01Source Title
Molecular & cellular oncologyPublisher
TAYLOR & FRANCIS INCAffiliation
Sir Peter MacCallum Department of OncologySurgery (St Vincent's)
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Journal ArticleCitations
Clemons, 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 Status
Open AccessNHMRC Grant code
NHMRC/1120293Abstract
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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