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The cis decoy against the estrogen response element suppresses breast cancer cells via target disrupting c-fos not mitogen- activated protein kinase activity

  1. Author:
    Wang, L. H.
    Yang, X. Y.
    Zhang, X. H.
    Mihalic, K.
    Xiao, W. H.
    Farrar, W. L.

  2. Author Address

    NCI, Intramural Res Support Program, Sci Applicat Int Corp, POB B,Bldg 560,Room 31-76, Frederick, MD 21702 USA NCI, Intramural Res Support Program, Sci Applicat Int Corp, Frederick, MD 21702 USA NCI, Cytokine Mol Mech Sect, Lab Mol Immunoregulat, NIH, Frederick, MD 21702 USA Wang LH NCI, Intramural Res Support Program, Sci Applicat Int Corp, POB B,Bldg 560,Room 31-76, Frederick, MD 21702 USA
    1. Year: 2003
  2. Journal: Cancer Research
    1. 63
    2. 9
    3. Pages: 2046-2051
  4. Type of Article: Article
  1. Abstract:

    Breast cancer, the most common malignancy in women, has been demonstrated to be associated with the steroid hormone estrogen and its receptor (ER), a ligand-activated transcription factor. Therefore, we developed a phosphorothiolate cis-element decoy against the estrogen response element (ERE decoy) to target disruption of ER DNA binding and transcriptional activity. Here, we showed that the ERE decoy potently ablated the 17beta- estrogen-inducible cell proliferation and induced apoptosis of human breast carcinoma cells by functionally affecting expression of c-fos gene and AP-1 luciferase gene reporter activity. Specificity of the decoy was demonstrated by its ability to directly block ER binding to a cis-element probe and transactivation. Moreover, the decoy failed to inhibit ER- mediated mitogen-activated protein kinase signaling pathways and cell growth of ER-negative breast cancer cells. Taken together, these data suggest that estrogen-mediated cell growth of breast cancer cells can be preferentially restricted via targeted disruption of ER at the level of DNA binding by a novel and specific decoy strategy applied to steroid nuclear receptors.

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