title: Suppression of KIF3B expression inhibits human hepatocellular carcinoma proliferation.
abstract: BACKGROUND
  Human hepatocellular carcinoma (HCC) is one of the most common fatal cancers and an important health problem worldwide, but its mechanism is still unclear. Microtubule (MT) kinesin motor proteins orchestrate a variety of cellular processes (e.g. mitosis, motility and organelle transportation) and have been involved in human carcinogenesis. KIF3B, the kinesin superfamily of proteins (KIFs), plays an important role in the regulation of mitotic progression.
  
  
  OBJECTIVE
  The expression of KIF3B and its involvement in HCC was investigated.
  
  
  METHODS
  Western blot and immunohistochemistry were used to measure the expression of KIF3B protein in HCC and adjacent non-tumorous tissues in 57 patients and Cell Counting Kit-8 to analyze the effects of growth and interference of KIF3B in the cell cycle process.
  
  
  RESULTS
  KIF3B protein level was increased in HCC tissues compared with the adjacent non-tumorous tissues. It was significantly associated with histological differentiation, tumor size, the level of alpha fetal protein (AFP) and proliferation marker Ki-67. Over-expression of KIF3B was correlated with poor survival. Following release of HepG2 cells from serum starvation, the expression of KIF3B was up-regulated. Furthermore, suppression of KIF3B not only decreased cancer cell growth but also induced apoptosis of cells.
  
  
  CONCLUSIONS
  Our results suggested that KIF3B expression was upregulated in HCC tumor tissues and proliferating HCC cells, and an increased KIF3B expression was associated with poor overall survival. KIF3B over-expression is involved in the pathogenesis of hepatocellular carcinoma and may serve as a potential therapeutic target for human HCC.
authors.affiliation: Department of Pathology, Nantong University Cancer Hospital, Nantong, 226001, Jiangsu, People's Republic of China.
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Huang
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.forename: Changlai
authors.initials: C
authors.lastname: Zhu
authors.forename: Jing
authors.initials: J
authors.lastname: Cai
authors.forename: Hua
authors.initials: H
authors.lastname: Wang
authors.forename: Xinxiu
authors.initials: X
authors.lastname: Wang
authors.forename: Song
authors.initials: S
authors.lastname: He
authors.forename: Cheng
authors.initials: C
authors.lastname: Liu
authors.forename: Li
authors.initials: L
authors.lastname: Yao
authors.forename: Zongmei
authors.initials: Z
authors.lastname: Ding
authors.forename: Yixin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Tianyi
authors.initials: T
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000502:physiology; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000378:metabolism / Q000401:mortality / Q000473:pathology; D002454:Cell Differentiation / Q000187:drug effects*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology*; D056945:Hep G2 Cells; D006801:Humans; D015151:Immunoblotting; D007150:Immunohistochemistry; D053208:Kaplan-Meier Estimate; D019394:Ki-67 Antigen / Q000378:metabolism; D016547:Kinesins / Q000235:genetics* / Q000378:metabolism*; D008113:Liver Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000401:mortality / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011379:Prognosis; D034741:RNA, Small Interfering / Q000502:physiology; D015854:Up-Regulation / Q000502:physiology; D055815:Young Adult
chemical_list: C095899:KIF3B protein, human; D019394:Ki-67 Antigen; D034741:RNA, Small Interfering; D016547:Kinesins