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- W2892559611 abstract "Abstract Melanoma patients frequently express functionally inactive tumor suppressor protein p53 harboring wild-type genotype (WTp53). A phosphorylated nuclear iASPP (inhibitor of apoptosis stimulating protein of p53) occurs in WTp53-expressing melanoma cells and metastatic tissues, and is associated with poor patient survival. The phosphorylation of iASPP is controlled by cyclin B1/cdk1 (cyclin-dependent kinase 1); in turn, phospho-iASPP inhibits multiple WTp53-dependent cellular events. We propose to reactivate WTp53 function/activity by control of iASPP using resveratrol and its high-affinity target protein quinone reductase 2 (NQO2). First, resveratrol inhibits melanoma cell proliferation and up-regulates p53 levels. Second, resveratrol restores p53 function and signaling by abrogating cyclin B1/cdk1-mediated iASPP phosphorylation. Correspondingly, NQO2 protects 20S proteasome-mediated p53 degradation. Treatment of melanoma via iASPP phosphorylation blockade to reinstate WTp53 function is novel. The use of resveratrol to regulate iASPP phosphorylation and WTp53 stability reinforces the possible use of dietary agents to treat melanoma patients expressing inactive WTp53." @default.
- W2892559611 created "2018-10-05" @default.
- W2892559611 creator A5006685141 @default.
- W2892559611 creator A5058325183 @default.
- W2892559611 creator A5068782556 @default.
- W2892559611 date "2018-01-01" @default.
- W2892559611 modified "2023-10-18" @default.
- W2892559611 title "An Outside-In and a Reciprocal Inside-Out Hypothesis Combining Resveratrol and Its High Affinity Protein NQO2 to Target iASPP for Reinstating the Activation and Stabilization of Dysfunctional WTp53 as a Melanoma Chemopreventive Approach" @default.
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- W2892559611 doi "https://doi.org/10.1016/b978-0-12-813008-7.00014-x" @default.
- W2892559611 hasPublicationYear "2018" @default.
- W2892559611 type Work @default.