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    Peroxiredoxin-3 is overexpressed in prostate cancer and promotes cancer cell survival by protecting cells from oxidative stress.

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    Authors
    Whitaker, H
    Patel, D
    Howat, W
    Warren, A
    Kay, J
    Sangan, T
    Marioni, J
    Mitchell, J
    Aldridge, S
    Luxton, H J
    Massie, C
    Lynch, A
    Neal, D
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    Affiliation
    Uro-Oncology Research Group, Cambridge CB2 0RE, UK.
    Issue Date
    2013-08-20
    
    Metadata
    Show full item record
    Abstract
    Objective:We have previously identified peroxiredoxin-3 (PRDX-3) as a cell-surface protein that is androgen regulated in the LNCaP prostate cancer (PCa) cell line. PRDX-3 is a member of the peroxiredoxin family that are responsible for neutralising reactive oxygen species.Experimental design:PRDX-3 expression was examined in tissue from 32 patients using immunohistochemistry. Subcellular distribution was determined using confocal microscopy. PRDX-3 expression was determined in antiandrogen-resistant cell lines by western blotting and quantitative RT-PCR. The pathways of PRDX-3 overexpression and knockdown on apoptosis and response to oxidative stress were investigated using protein arrays.Results:PRDX-3 is upregulated in a number of endocrine-regulated tumours; in particular in PCa and prostatic intraepithelial neoplasia. Although the majority of PRDX-3 is localised to the mitochondria, we have confirmed that PRDX-3 at the cell membrane is androgen regulated. In antiandrogen-resistant LNCaP cell lines, PRDX-3 is upregulated at the protein but not RNA level. Resistant cells also possess an upregulation of the tricarboxylic acid (TCA) pathway and resistance to H2O2-induced apoptosis through a failure to activate pro-apoptotic pathways. Knockdown of PRDX-3 restored H2O2 sensitivity.Conclusion:Our results suggest that PRDX-3 has an essential role in regulating oxidation-induced apoptosis in antiandrogen-resistant cells. PRDX-3 may have potential as a therapeutic target in castrate-independent PCa.
    Citation
    Peroxiredoxin-3 is overexpressed in prostate cancer and promotes cancer cell survival by protecting cells from oxidative stress. 2013, 109 (4):983-93 Br J Cancer
    Journal
    British Journal of Cancer
    URI
    http://hdl.handle.net/10541/302806
    DOI
    10.1038/bjc.2013.396
    PubMed ID
    23880827
    Type
    Article
    Language
    en
    ISSN
    1532-1827
    ae974a485f413a2113503eed53cd6c53
    10.1038/bjc.2013.396
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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