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  • Title: Restoration of cyclin D2 has an inhibitory potential on the proliferation of LNCaP cells.
    Author: Kobayashi T, Nakamura E, Shimizu Y, Terada N, Maeno A, Kobori G, Kamba T, Kamoto T, Ogawa O, Inoue T.
    Journal: Biochem Biophys Res Commun; 2009 Sep 11; 387(1):196-201. PubMed ID: 19577536.
    Abstract:
    Despite well known oncogenic function of G1-S cell-cycle progression, cyclin D2 (CCND2) is often silenced epigenetically in prostate cancers. Here we show that CCND2 has an inhibitory potential on the proliferation of androgen receptor (AR)-dependent prostate cancer LNCaP cells. Forced expression of CCND2 suppressed the proliferative ability and induced cell death in LNCaP cells in a cdk-independent manner. Knocking down CCND2 restored the proliferation of LNCaP subclones with relatively high CCND2 expression and low proliferative profiles. Immunoprecipitation using deletion mutants of CCND2 indicated that a central domain of CCND2 is required for binding to AR. A deletion mutant lacking the central domain failed to hinder LNCaP cells. Collectively, our results indicated that CCND2 inhibits cell proliferation of AR-dependent prostate cancer through the interaction with AR. Our study suggests that restoration of CCND2 expression potentially prevents the carcinogenesis of prostate cancer, which is mostly AR-dependent in the initial settings.
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