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Lack of p53-mediated G1 arrest in response to an environmental carcinogen

  1. Author:
    Khan, Q. A.
    Vousden, K. H.
    Dipple, A.

  2. Author Address

    Khan QA NCI, Frederick Canc Res & Dev Ctr, Chem Carcinogenesis Lab, ABL Basic Res Program Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Chem Carcinogenesis Lab, ABL Basic Res Program Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Mol Virol & Carcinogenesis Lab, ABL Basic Res Program Frederick, MD 21702 USA
    1. Year: 1999
  2. Journal: Oncology (Huntington)
    1. 57
    2. 3
    3. Pages: 258-264
  4. Type of Article: Article
  1. 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 DMA 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. [References: 34]

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