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• W2101292261 abstract "Abstract Mutant p53 is a cancer-specific target for pharmacologic intervention. We show that histone deacetylase inhibitors such as FR901228 and trichostatin A completely depleted mutant p53 in cancer cell lines. This depletion was preceded by induction of p53-regulated transcription. In cells with mutant p53 pretreated with histone deacetylase inhibitors, DNA damage further enhanced the p53 trans-function. Furthermore, histone deacetylase inhibitors were preferentially cytotoxic to cells with mutant p53 rather than to cells lacking wild-type p53. We suggest that, by either restoring or mimicking p53 trans-functions, histone deacetylase inhibitors initiate degradation of mutant p53. Because mutant p53 is highly expressed, a sudden restoration of p53-like functions is highly cytotoxic to cells with mutant p53. In a broader perspective, this shows how selectivity may be achieved by targeting a non-cancer-specific target, such as histone deacetylases, in the presence of a cancer-specific alteration, such as mutant p53." @default.
• W2101292261 created "2016-06-24" @default.
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• W2101292261 date "2005-08-15" @default.
• W2101292261 modified "2023-10-16" @default.
• W2101292261 title "Depletion of Mutant p53 and Cytotoxicity of Histone Deacetylase Inhibitors" @default.
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• W2101292261 doi "https://doi.org/10.1158/0008-5472.can-04-3433" @default.
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