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- W2009459879 abstract "It has been shown that isothiocyanates (ITCs), derived from hydrolysis of glucosinolates in cruciferous vegetables via Lossen rearrangement by myrosinase, induce apoptosis in cancer cells. We here demonstrate that certain naturally-occurring ITCs selectively deplete mutant p53, but not the wild type, and do so via a post-transcriptional mechanism. Direct p53 binding and the sequential conformational changes appears to be one of the mechanisms by which mutant p53 is depleted. Structure-activity relationship studies (SARs) using naturally-occurring and synthetic ITCs show that depletion is influenced by the structure of the ITC side chain moiety. Consistent with the gain of function by mutant p53, we show that cells with p53 mutations are more sensitive to the cytotoxicity of phenethylisothiocyanate (PEITC) than are those with the wild type. Furthermore, 2,2-diphenylethyl ITC, a synthetic ITC and one of the most potent depletors of mutant p53 studied, induces apoptosis to the greatest extent in breast cancer cells with mutant p53 status. Collectively, this study shows that mutant p53 depletion may be an important novel target for cancer chemoprevention and therapy by natural and synthetic ITCs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3691. doi:10.1158/1538-7445.AM2011-3691" @default.
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- W2009459879 date "2011-04-15" @default.
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- W2009459879 title "Abstract 3691: Selective depletion of mutant p53 by isothiocyanates and its structure-activity relationships" @default.
- W2009459879 doi "https://doi.org/10.1158/1538-7445.am2011-3691" @default.
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