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    Aspirin and alterations in DNA repair proteins in the SW480 colorectal cancer cell line.

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    Authors
    Dibra, H. K.
    Brown, J. E.
    Hooley, Paul
    Nicholl, I. D.
    Issue Date
    2010
    
    Metadata
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    Abstract
    Regular aspirin intake is associated with a reduction in the incidence of colorectal cancer. Aspirin has been shown to be cytotoxic to colorectal cancer cells in vitro. The molecular basis for this cytotoxicity is controversial, with a number of competing hypotheses in circulation. One suggestion is that the protective effect is related to the induction of expression of the DNA mismatch repair (MMR) proteins hMLH1, hMSH2, hMSH6 and hPMS2 in DNA MMR proficient cells. We report that treatment of the DNA MMR competent/p53 mutant colorectal cancer cell line SW480 with 1 mM aspirin for 48 h caused changes in mRNA expression of several key genes involved in DNA damage signalling pathways, including a significant down-regulation in transcription of the genes ATR, BRCA1 and MAPK12. Increases in the transcription of XRCC3 and GADD45alpha genes are also reported. Regulation of these genes could potentially have profound effects on colorectal cancer cells and may play a role in the observed chemo-protective effect of aspirin in vivo. Although a correlation was not seen between transcript and protein levels of ATR, BRCA1 and GADD45alpha, an increase in XRCC3 encoded protein expression upon aspirin treatment in SW480 cells was observed by immunoblotting, immunofluorescence and immunohistochemical analysis. This is the first report of XRCC3 gene transcription and encoded protein expression being susceptible to exposure to the non-steroidal anti-inflammatory drug, aspirin. Furthermore, this study indicates that alterations in gene transcription seen in microarray studies must be verified at the protein level.
    Citation
    Oncology reports, 24 (1):37-46
    Publisher
    Spandios Publications
    Journal
    Oncology reports
    URI
    http://hdl.handle.net/2436/117148
    DOI
    10.3892/or_00000826
    PubMed ID
    20514442
    Type
    Journal article
    Language
    en
    ISSN
    1791-2431
    ae974a485f413a2113503eed53cd6c53
    10.3892/or_00000826
    Scopus Count
    Collections
    Faculty of Science and Engineering

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