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

      Cancer Cell

      Animals, Cell Line, Tumor, Cell Transformation, Neoplastic, DNA-Binding Proteins, metabolism, Gene Silencing, Genomics, Humans, Male, Mice, Mice, Inbred BALB C, Models, Biological, Neoplasm Transplantation, Polycomb Repressive Complex 2, Promoter Regions, Genetic, Prostatic Neoplasms, genetics, Receptors, Adrenergic, beta-2, physiology, Transcription Factors

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          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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          Journal
          17996646
          10.1016/j.ccr.2007.10.016

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