title: Livin-α promotes cell proliferation by regulating G1-S cell cycle transition in prostate cancer.
abstract: 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.
authors.affiliation: Department of Urology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Ye
authors.forename: Xishuang
authors.initials: X
authors.lastname: Song
authors.forename: Sheng
authors.initials: S
authors.lastname: Li
authors.forename: Deyong
authors.initials: D
authors.lastname: Yang
authors.forename: Jianing
authors.initials: J
authors.lastname: Zhang
authors.forename: Xiangyu
authors.initials: X
authors.lastname: Che
authors.forename: Xiaochi
authors.initials: X
authors.lastname: Chen
authors.forename: Jianbo
authors.initials: J
authors.lastname: Wang
authors.forename: Zhiwei
authors.initials: Z
authors.lastname: Zhang
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000502:physiology*; D000230:Adenocarcinoma / Q000473:pathology*; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000502:physiology*; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D009363:Neoplasm Proteins / Q000502:physiology*; D011470:Prostatic Hyperplasia / Q000378:metabolism / Q000473:pathology*; D011471:Prostatic Neoplasms / Q000378:metabolism / Q000473:pathology*; D020033:Protein Isoforms / Q000502:physiology
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C419866:BIRC7 protein, human; D051034:Inhibitor of Apoptosis Proteins; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D020033:Protein Isoforms