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• W1966592073 abstract "The environmental carcinogen, 5-methylchrysene, is a component of cigarette smoke. Its reactive metabolite, anti-5-methylchrysene-1, 2-dihydrodiol-3,4-epoxide (5-MeCDE) mainly reacts with the N(2)-position of guanine residues in the DNA molecule. In this study, we demonstrate that the tumor suppressor protein p53 is stabilized in response to DNA damage by 5-MeCDE but fails to induce the cells' protective mechanism of G1 arrest in the human breast carcinoma cell line, MCF-7. In contrast, actinomycin D treatment of these cells did lead to G1 arrest. Western analyses revealed that, though both actinomycin D and 5-MeCDE treatment stabilized p53, only trace levels of p21(waf1/cip1) were seen in the latter case. This lack of p21(waf1/cip1) expression in 5-MeCDE-treated cells is attributed to a stealth characteristic of this environmental carcinogen that allows it to damage DNA and still escape the p53-mediated cellular defense mechanism of G1 arrest." @default.
• W1966592073 created "2016-06-24" @default.
• W1966592073 creator A5046738539 @default.
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• W1966592073 date "1999-01-01" @default.
• W1966592073 modified "2023-09-26" @default.
• W1966592073 title "Lack of p53-Mediated G1 Arrest in Response to an Environmental Carcinogen" @default.
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• W1966592073 doi "https://doi.org/10.1159/000012040" @default.
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