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    VEGF/Neuropilin-2 Regulation of Bmi-1 and Consequent Repression of IGF-IR Define a Novel Mechanism of Aggressive Prostate Cancer

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    Authors
    Goel, Hira Lal
    Chang, Cheng
    Pursell, Bryan M.
    Leav, Irwin
    Lyle, Stephen
    Xi, Hualin Simon
    Hsieh, Chung-Cheng
    Adisetiyo, Helty
    Roy-Burman, Pradip
    Coleman, Ilsa M.
    Nelson, Peter S.
    Vessella, Robert L.
    Davis, Roger J.
    Plymate, Stephen R.
    Mercurio, Arthur M.
    Show allShow less
    UMass Chan Affiliations
    Program in Molecular Medicine
    Department of Cancer Biology
    Document Type
    Journal Article
    Publication Date
    2012-10-01
    Keywords
    Biochemistry
    Cancer Biology
    Cell Biology
    Molecular Biology
    Neoplasms
    
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4205964/
    Abstract
    We show that the VEGF receptor neuropilin-2 (NRP2) is associated with high-grade, PTEN-null prostate cancer and that its expression in tumor cells is induced by PTEN loss as a consequence of c-Jun activation. VEGF/NRP2 signaling represses insulin-like growth factor-1 receptor (IGF-IR) expression and signaling, and the mechanism involves Bmi-1-mediated transcriptional repression of the IGF-IR. This mechanism has significant functional and therapeutic implications that were evaluated. IGF-IR expression positively correlates with PTEN and inversely correlates with NRP2 in prostate tumors. NRP2 is a robust biomarker for predicting response to IGF-IR therapy because prostate carcinomas that express NRP2 exhibit low levels of IGF-IR. Conversely, targeting NRP2 is only modestly effective because NRP2 inhibition induces compensatory IGF-IR signaling. Inhibition of both NRP2 and IGF-IR, however, completely blocks tumor growth in vivo.
    Source

    Cancer Discov. 2012 Oct;2(10):906-921. Epub 2012 Jul 9. Link to article on publisher's site

    DOI
    10.1158/2159-8290.CD-12-0085
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/26293
    PubMed ID
    22777769
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1158/2159-8290.CD-12-0085
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