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    The effects of phenoxodiol on the cell cycle of prostate cancer cell lines

    219300_144454_2014_Phenoxodiol_and_Prostate.pdf (1.082Mb)
    Access Status
    Open access
    Authors
    Mahoney, S.
    Arfuso, Frank
    Millward, M.
    Dharmarajan, A.
    Date
    2014
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Mahoney, S. and Arfuso, F. and Millward, M. and Dharmarajan, A. 2014. The effects of phenoxodiol on the cell cycle of prostate cancer cell lines. Cancer Cell International. 14 (110): pp. 1-12.
    Source Title
    Cancer Cell International
    DOI
    10.1186/s12935-014-0110-z
    ISSN
    1475-2867
    School
    School of Biomedical Sciences
    Remarks

    This article is published under the Open Access publishing model and distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/. Please refer to the licence to obtain terms for any further reuse or distribution of this work.

    URI
    http://hdl.handle.net/20.500.11937/16583
    Collection
    • Curtin Research Publications
    Abstract

    Background: Prostate cancer is associated with a poor survival rate. The ability of cancer cells to evade apoptosis and exhibit limitless replication potential allows for progression of cancer from a benign to a metastatic phenotype. The aim of this study was to investigate in vitro the effect of the isoflavone phenoxodiol on the expression of cell cycle genes. Methods: Three prostate cancer cell lines-LNCaP, DU145, and PC3 were cultured in vitro, and then treated with phenoxodiol (10 μM and 30 μM) for 24 and 48 h. The expression of cell cycle genes p21WAF1, c-Myc, Cyclin-D1, and Ki-67 was investigated by Real Time PCR. Results: Here we report that phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle, with the resultant arrest due to the upregulation of p21WAF1 in all the cell lines in response to treatment, indicating that activation of p21WAF1 and subsequent cell arrest was occurring via a p53 independent manner, with induction of cytotoxicity independent of caspase activation. We found that c-Myc and Cyclin-D1 expression was not consistently altered across all cell lines but Ki-67 signalling expression was decreased in line with the cell cycle arrest. Conclusions: Phenoxodiol demonstrates an ability in prostate cancer cells to induce significant cytotoxicity in cells by interacting with p21WAF1 and inducing cell cycle arrest irrespective of p53 status or caspase pathway interactions. These data indicate that phenoxodiol would be effective as a potential future treatment modality for both hormone sensitive and hormone refractory prostate cancer.

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