Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage
Cell ResearchPublished 3 April 2007
Yu-Ting Lin, Junichi Fukuchi, Richard A. Hiipakka, John M. Kokontis, Jialing Xiang
Citations107
SJR quartileQ1
SJR score8.74
SNIP3.79
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TL;DR
It is reported that Bcl-2 is required for the progression of LNCaP prostate cancer cells from an androgens-dependent to an androgen-independent growth stage and shRNA-mediated gene silencing of Bcl1 promotes UV-induced apoptosis and suppresses the growth of prostate tumors in vivo.
Abstract
Bcl-2 is an anti-apoptotic oncoprotein and its protein levels are inversely correlated with prognosis in many cancers. However, the role of Bcl-2 in the progression of prostate cancer is not clear. Here we report that Bcl-2 is required for the progression of LNCaP prostate cancer cells from an androgen-dependent to an androgen-independent growth stage. The mRNA and protein levels of Bcl-2 are significantly increased in androgen-independent prostate cancer cells. shRNA-mediated gene silencing of Bcl-2 in androgen-independent prostate cancer cells promotes UV-induced apoptosis and suppresses the growth of prostate tumors in vivo. Growing androgen-dependent cells under androgen-deprivation conditions results in formation of androgen-independent colonies; and the transition from androgen-dependent to androgen-independent growth is blocked by ectopic expression of the Bcl-2 antagonist Bax or Bcl-2 shRNA. Thus, our results demonstrate that Bcl-2 is not only critical for the survival of androgen-independent prostate cancer cells, but is also required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage.
Keywords
ChemistryMedicineBiochemistry, Genetics and Molecular Biology
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