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    PSA regulates androgen receptor expression in prostate cancer cells

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    Authors
    Saxena, Parmita
    Trerotola, Marco
    Wang, Tao
    Li, Jing
    Sayeed, Aejaz
    Vanoudenhove, Jennifer
    Adams, Dave S.
    Fitzgerald, Thomas J.
    Altieri, Dario C.
    Languino, Lucia R.
    UMass Chan Affiliations
    Department of Cancer Biology, Department of Radiation Oncology,
    Document Type
    Journal Article
    Publication Date
    2012-05-15
    Keywords
    Cell Line, Tumor
    Down-Regulation
    Humans
    Male
    Metribolone
    Neoplasms, Hormone-Dependent
    Phosphorylation
    Prostate-Specific Antigen
    Prostatic Neoplasms
    Proto-Oncogene Proteins pp60(c-src)
    Receptors, Androgen
    Neoplasms
    Oncology
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    Link to Full Text
    http://dx.doi.org/10.1002/pros.21482
    Abstract
    BACKGROUND: Prostate-specific antigen (PSA) is a pivotal downstream target gene of the androgen receptor (AR), and a serum biomarker to monitor prostate cancer (PrCa) progression. It has been reported that PSA transactivates AR, but the mechanistic requirements of this response have not been investigated. METHODS: We studied the localization of PSA, AR, and Src in intracellular compartments of synthetic androgen (R1881)-stimulated LNCaP and C4-2B PrCa cells, using immunofluorescence and subcellular fractionation approaches. We also investigated the effect of downregulation of PSA on AR expression by immunoblotting and real-time PCR using short hairpin RNA (shRNA) and small interfering RNA (siRNA). Src activity was analyzed by immunoblotting. RESULTS: R1881 stimulation induced nuclear localization of both PSA and AR in LNCaP and C4-2B PrCa cells as well as increased phosphorylation of Src. Stable shRNA or transient siRNA knockdown of PSA resulted in reduced AR protein levels as well as AR mRNA levels in C4-2B cells. Similar to C4-2B cells, ablation of AR levels upon silencing of PSA was also confirmed in VCaP cells, another androgen-independent cell line. Silencing of PSA did not cause significant changes in Src activation; besides, Src regulation by integrins did not appear to affect AR transcriptional activity. CONCLUSIONS: PSA localizes to nuclei of androgen-stimulated PrCa cells, and controls AR mRNA and protein levels. This regulatory loop is specific for PSA, does not involve known AR activators such as Src and AKT, and may contribute to AR signaling under conditions of increasing PSA levels in patients.
    Source
    Prostate. 2012 May 15;72(7):769-76. doi: 10.1002/pros.21482. Epub 2011 Sep 28. Link to article on publisher's site
    DOI
    10.1002/pros.21482
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/47935
    PubMed ID
    21956655
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1002/pros.21482
    Scopus Count
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    Radiation Oncology Publications

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