摘要
目的:利用构建好的GPC3真核表达载体,探讨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倍目镜下基因转染组细胞的穿膜细胞数为131.7±7.44。空质粒转染组细胞的穿膜细胞数为71.6±4.76。侵袭实验中,200倍目镜下基因转染组细胞的穿膜细胞数为220±12.8。空质粒转染组细胞的穿膜细胞数为138±10.5。两组细胞比较,迁移、侵袭能力均显著增强(P<0.001)。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： SK - Hep - 1 cell were transfected with pEGFP - N2 - GPC3, and study its role on proliferation, adhesion and invasion of SK - Hep- 1 hepatoma carcinoma cells. Method： SK- Hep- 1 cell were transfected with pEGFP- N2 - GPC3 using Lipofeetamine2000. After GPC3 was transfected into SK - Hep- 1 eeUs successfully, Growth velocity, ability of cell adhesion, migration and invasion were observed. Results： Forced expression of GPC3 suppresses the growth of SK - Hep- 1 cells. Forced expression of GPC3 reduces adhesion capacity. In migration experiment, the trans - membrane cen numbers in GPC3 trans- feeted SK- Hep- 1 hepatoma carcinoma cells were （131.7 ± 7.44） /HT, and in blank plasrnid transfeeted cells were （71.6 ± 4.76） /HT. In invasion experiment, the trans-membrane cell numbers in GPC3 transfected SK- Hep- 1 hepatoma carcinoma cells were （220 ± 12.8） /HT, and in blank plasmid transfected ceils were （138 ±10.5 ） /HT. There was significant difference between the two groups （P〈 0.001 ） . Conclusion： Forced expression of GPC3 suppresses the growth of SK - Hep - 1 cells. Forced expression of GPC3 reduces adhesion capacity, but stimulates migration and invasiveness.
出处
《福州总医院学报》
2010年第1期16-18,51,共4页
Journal of Fuzhou General Hospital
基金
福建省青年科技人才创新项目(2005J074)
