GPC3基因对人肝癌细胞SK-Hep-1生物学行为的影响

Role of pEGFP-N2-GPC3 expression vector in SK-Hep-1 hepatoma carcinoma cancer cell

目的:利用构建好的GPC3真核表达载体,研究其对肝癌细胞生物学行为的影响。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,观察转染前后肝癌细胞增殖、黏附、运动及体外侵袭能力的改变,并观察四种生长因子FGF2、IGF2、BMP4、TGFβ1对GPC3抑制细胞增殖的影响。结果:GPC3抑制SK-Hep-1的增殖,降低对Matrigel胶的黏附能力,增加SK-Hep-1的迁移及侵袭能力,GPC3抑制FGF2对SK-Hep-1细胞的增殖效应,而对其他三种生长因子IGF2、BMP4、TGFβ1无此作用。结论:GPC3真核表达载体可抑制肝癌细胞SK-Hep-1的增殖,但可降低其对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信号途径来抑制肝癌细胞细胞的增殖。

Objective： SK- Hep - 1 cell were transfected with pEGFP - N2 - GPC3, and study its role on the biological behaviors of SK - Hep- 1 hepatoma carcinoma cells. Method： SK - Hep- 1 cell were transfected with pEGFP- N2 - GPC3 using Lipofectamine2000. After GPC3 was transfected into SK - Hep - 1 cells successfully, The growth velocity and the ability of cell adhesion, cell migration, cell invasion before and after transfection was observe, the effects of various growth factors, including FGF2, IGF2, BMP4 and TGFβI, on GPC3 - SK - Hep - 1 were analyzed. Results： Forced expression of GPC3 suppresses the growth of SK - Hep - 1 cells. Forced expression of GPC3 reduces adhesion capacity, but stimulates migration and invasiveness. FGF2 - induced cell proliferation proved to be significantly decreased by GPC3, whereas the growth effects of IGF2, BMP4, and TGFβ1 were not altered by GPC3. Conclusion： Forced expression of GFC3 suppresses the growth of SK- Hep- 1 cells. Forced expression of GPC3 reduces adhesion capacity, but stimulates migration and invasiveness. Forced expression of GPC3 modulates FGF2 signaling.