基础医学与临床 ›› 2014, Vol. 34 ›› Issue (3): 376-380.

• 研究论文 • 上一篇    下一篇

CCN5对肝癌细胞系HepG2增殖、迁移和侵袭能力的影响及其作用机制

李海军,孟宪飞,董志意,刘亚峰   

  1. 榆林市第一医院
  • 收稿日期:2013-05-16 修回日期:2013-09-25 出版日期:2014-03-05 发布日期:2014-02-27
  • 通讯作者: 李海军 E-mail:lihaijun161@163.com

Effect of CCN5 on proliferation, migration and invasion of hepatoma carcinoma cells and the mechanism

  • Received:2013-05-16 Revised:2013-09-25 Online:2014-03-05 Published:2014-02-27

摘要: 目的 研究CCN5过表达对人肝癌细胞增殖、迁移和侵袭能力的影响及其作用机制。方法 以人HepG2细胞为研究对象,构建CCN5过表达载体,转染人HepG2细胞,使CCN5在人HepG2细胞中过表达,分别采用细胞增殖检测试剂盒、Transwell小室法观察其对HepG2细胞增殖、迁移及侵袭能力的影响;采用Western blot检测Smad2及p44/42MAPK磷酸化水平。结果 CCN5成功在人HepG2细胞中过表达,较对照组,CCN5过表达组,细胞增殖、迁移及侵袭能力相比受到明显抑制(P<0.05);Smad2及phospho-p44/42磷酸化水平也受到明显抑制。结论 CCN5过表达可抑制人肝癌的形成。

关键词: CCN5, 肝癌细胞, 增殖, 迁移, 侵袭

Abstract: Objective To study the effect of CCN5 on proliferation, migration and invasion of hepatoma carcinoma cells and the mechanism. Methods Hepatocyte High Expression System of CCN5 was constructed and transfected HepG2 cells to make CCN5 overexpression, and then cell proliferation detection reagent box and Transwell chamber were used to determine the effect of CCN5 overexpression on proliferation, migration and invasion of HepG2. To further study the mechanism, phosphorylation levels of Smad2 and p44/42MAPK were determined. Results CCN5 was overexpressed in HepG2 cells. After that, the proliferation, migration and invasion of the CCN5 overexpression group were significantly inhibited (P <0.05) compared with the normal control group. Phosphorylation levels of Smad2 and p44/42MAPK were also significantly inhibited. Conclusion Overexpression of CCN5 can inhibit proliferation, migration and invasion of HepG2, which plays an important role in the formation of human hepatoma and proposes a new idea for the prevention and treatment of hepatic carcinoma.

Key words: CCN5, Hepatoma carcinoma cell, Proliferation, Migration, Invasion