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Livin‐α promotes cell proliferation by regulating G 1 ‐S cell cycle transition in prostate cancer
Author(s) -
Ye Lin,
Song Xishuang,
Li Sheng,
Yang Deyong,
Zhang Jianing,
Che Xiangyu,
Chen Xiaochi,
Wang Jianbo,
Zhang Zhiwei
Publication year - 2010
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.21220
Subject(s) - lncap , prostate cancer , cancer research , cell growth , cancer , cell cycle , proliferation index , medicine , biology , biochemistry
BACKGROUND Prostate cancer is the third most common cancer and the second leading cause of cancer death for males in US. Livin has recently been described as a cancer‐associated member of inhibitor of apoptosis proteins family, highly expressed in prostate cancer. Livin gene encodes two splicing variants, termed Livin‐α and Livin‐β. We hypothesized that deregulation of proliferation could be due in part to Livin expression. METHODS Pathological analysis of Livin was performed in 20 prostate cancer tissues and 5 benign prostatic hyperplasia tissues. The expression of Livin isoforms was also investigated by Western blot in prostate cancer cell lines LNCaP and PC3. The role of Livin‐α in vitro was further studied. Using Livin‐α knockdown and overexpression models, cell cycle analysis, Ki‐67 immunocytostaining, and MTT assay were performed respectively. RESULTS Livin expression positive ratio was shown to be 5.4%, 23.6%, 52.4%, 73.4% in benign prostatic hyperplasia, low, medium, and high grade of prostate cancer respectively, and Livin was positively correlated with clinical pathological grades of prostate cancer. Livin‐α was expressed in both LNCaP and PC3; meanwhile; Livin‐β was only detected in the PC3. Livin‐α siRNA not only resulted in G 1 ‐S cell cycle arrest, but also strongly correlated with the descended proliferation index and survival rate in LNCaP. In comparison, overexpression of Livin‐α resulted in an accelerated S phase entry combined with elevated proliferation index and survival in LNCaP. CONCLUSIONS Livin‐α may promote cell proliferation by regulating G 1 ‐S cell cycle transition and possibly play an important part in initiation of prostate cancer. Prostate 71: 42–51, 2011. © 2010 Wiley‐Liss, Inc.