摘要
目的利用构建好的GPC3真核表达载体，观察GPC3基因对SK-Hep-1肝癌细胞增殖、黏附、侵袭能力的影响。方法将pEGFP-N2-GPC3增强型绿色荧光蛋白表达载体通过脂质体方法转入SK-Hep-1人肝癌细胞，确定GPC3已经成功转入细胞后，观察肝癌细胞转染前后增殖、黏附、迁移及侵袭能力的改变。结果GPC3抑制SK-Hep-1的增殖，降低对Matrigel胶的黏附能力，迁移实验中，200倍目镜下实验组细胞的穿膜细胞数为131．70±7．44。空质粒对照组细胞的穿膜细胞数为71．60±4．76。侵袭实验中，200倍目镜下实验组细胞的穿膜细胞数为220．00±12．80。空质粒对照组细胞的穿膜细胞数为138．00±10．50。两组细胞比较，迁移、侵袭能力均显著增强（P〈0．01）。结论GPC3真核表达载体抑制肝癌细胞SK-Hep-1的增殖，降低其对Matrigel胶的黏附能力，增加其迁移及侵袭能力，GPC3可能通过抑制FGF2信号途径抑制肝癌细胞的增殖。
Objective By using constructed GPC3 eukaryotic expression vector,to investigate the influence of GPC3 gene on proliferation, adhesion and invasion of SK-Hep-1 hepatoma carcinoma cells. Methods SK-Hep-1 cells were transfected with pEGFP-N2-GPC3 by using Lipofectamine2000. After GPC3 was transfected into SK-Hep-1 cells successfully, growth velocity, ability of cell adhesion, migration and invasion were observed. Results Forced expression of G-PC3 suppressed the growth of SK-Hep-1 cells and reduced adhesion capacity. In migration experiment, the trans-membrane cell number in GPC3 transfected SK-Hep-1 hepatoma carcinoma cells was （131.70±7.44）/HT, and that in blank plasmid transfected cells （71.60±4.76）/HT. In invasion experiment, the trans-membrane cell number in G-PC3 transfected SK-Hep-1 hepatoma carcinoma cells was （220. 130 ± 12.80 ）/HT, and that in blank plasmid transfected cells （138.130 ± 10.50）/HT. There was significant difference between the two groups （P 〈 0. 01 ）. Conclusion Forced expression of GPC3 suppresses the growth of SK-Hep-1 cells and reduces adhesion capacity,but stimulates migration and invasiveness.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2008年第9期1143-1145,F0003,共4页
Chinese Journal of Experimental Surgery
基金
福建省青年科技人才创新项目（2005J074）
