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'Stealth properties' contribute to the potent action of polycyclic aromatic hydrocarbon carcinogens

  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: Polycyclic Aromatic Compounds
    1. 16
    2. 1-4
    3. Pages: 89-98
  4. Type of Article: Article
  1. Abstract:

    Dihydrodiol epoxides are carcinogenic metabolites of polycyclic aromatic hydrocarbons. The effects of two such compounds, benzo[g]chrysene 11,12-dihydrodiol 13,14-epoxide and 5-methylchrysene 1,2-dihydrodiol 3,4-epoxide, on the progress of the human mammary carcinoma cell, MCF-7, through the cell cycle was investigated. Unlike other DNA damaging agents, such as actinomycin D, these carcinogens did not arrest MCF-7 cells in the G1 phase of the cell cycle and the cells began DNA replication despite the damage in the DNA template. The dihydrodiol epoxides, like actinomycin D, induced the p53 protein that normally mediates G1 arrest through transcriptional activation of p21(waf1/cip1), in these cells. However, increased cellular p21(waf1/cip1) levels were not found in the hydrocarbon-treated cells. Thus, these carcinogens did not trigger the major 'guardian of the genome' cellular defense mechanism mediated by p53. This stealth characteristic may be an important contributor to the carcinogenic action of these agents. [References: 31]

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