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Integrative genornics analysis reveals silencing of beta-adrenergic signaling by polycomb in prostate cancer

  1. Author:
    Yu, J.
    Cao, Q.
    Mehra, R.
    Laxman, B.
    Yu, J.
    Tomlins, S. A.
    Creighton, C. J.
    Dhanasekaran, S. M.
    Shen, R.
    Chen, G.
    Morris, D. S.
    Marquez, V. E.
    Shah, R. B.
    Ghosh, D.
    Varambally, S.
    Chinnaiyan, A. M.

  2. Author Address

    Univ Michigan, Sch Med, Dept Pathol, Michigan Ctr Translat Pathol, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Dept Urol, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Dept Biostat, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Bioinformat Program, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Dept Surg, Ann Arbor, MI 48109 USA. NCI, Med Chem Lab, Canc Res Ctr, NIH, Frederick, MD 21702 USA.;Chinnaiyan, AM, Univ Michigan, Sch Med, Dept Pathol, Michigan Ctr Translat Pathol, Ann Arbor, MI 48109 USA.;arul@umich.edu
    1. Year: 2007
    2. Date: Nov
  2. Journal: Cancer Cell
    1. 12
    2. 5
    3. Pages: 419-431
  4. Type of Article: Article
  5. ISSN: 1535-6108
  1. Abstract:

    The Polycomb group (PcG) protein EZH2 possesses oncogenic properties for which the underlying mechanism is unclear. We integrated in vitro cell line, in vivo tumor profiling, and genome-wide location data to nominate key targets of EZH2. One of the candidates identified was ADRB2 (Adrenergic Receptor, Beta-2), a critical mediator of beta-adrenergic signaling. EZH2 is recruited to the ADRB2 promoter and represses ADRB2 expression. ADRB2 inhibition confers cell invasion and transforms benign prostate epithelial cells, whereas ADRB2 overexpression counteracts EZH2-mediated oncogenesis. ADRB2 is underexpressed in metastatic prostate cancer, and clinically localized tumors that express lower levels of ADRB2 exhibit a poor prognosis. Taken together, we demonstrate the power of integrating multiple diverse genomic data to decipher targets of disease-related genes.

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External Sources

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  2. DOI: 10.1016/j.ccr.2007.10.016
  3. View record in Web of Science®
  4. WOS: 000251006900006

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