Suppression of KIF3B Expression Inhibits Human Hepatocellular Carcinoma Proliferation

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• 作者：Xiaodong Huang (2) (3)
  Fang Liu (1)
  Changlai Zhu (1)
  Jing Cai (2)
  Hua Wang (2)
  Xinxiu Wang (1)
  Song He (2)
  Cheng Liu (1)
  Li Yao (1)
  Zongmei Ding (1)
  Yixin Zhang (2)
  Tianyi Zhang (1)
  
• 关键词：Human hepatocellular carcinoma (HCC) ; KIF3B ; Cell proliferation ; Pathogenesis
• 刊名：Digestive Diseases and Sciences
• 出版年：2014
• 出版时间：April 2014
• 年：2014
• 卷：59
• 期：4
• 页码：795-806
• 全文大小：3,141 KB
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• 作者单位：Xiaodong Huang (2) (3)
  Fang Liu (1)
  Changlai Zhu (1)
  Jing Cai (2)
  Hua Wang (2)
  Xinxiu Wang (1)
  Song He (2)
  Cheng Liu (1)
  Li Yao (1)
  Zongmei Ding (1)
  Yixin Zhang (2)
  Tianyi Zhang (1)
  
  2. Department of Pathology, Nantong University Cancer Hospital, Nantong, 226001, Jiangsu, People鈥檚 Republic of China
  3. Department of Nutrition, Nantong University Hospital, Nantong, 226001, Jiangsu, People鈥檚 Republic of China
  1. Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001, Jiangsum, People鈥檚 Republic of China
  
• ISSN：1573-2568

文摘

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. Aim 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.