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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: To investigate the effect of GPC3 gene on the proliferation, adhesion and invasion of SK-Hep-1 hepatoma cells by using the constructed GPC3 eukaryotic expression vector. Methods: The EGFP-N2-GPC3 enhanced green fluorescent protein expression vector was transfected into SK-Hep-1 human hepatocellular carcinoma cells by lipofectamine. After GPC3 cells were successfully transfected into the cells, the proliferation, adhesion, Migration and change in ability to attack. Results: GPC3 could inhibit the proliferation of SK-Hep-1 and decrease the adhesive ability to Matrigel. The number of transmembrane cells in the transfection group was 131.7 ± 7.44. The number of transmembrane cells in the empty plasmid transfection group was 71.6 ± 4.76. In the invasion experiment, the number of transmembrane cells in cells transfected with 200-fold eyepiece was 220 ± 12.8. The number of transmembrane cells in the empty plasmid transfected group was 138 ± 10.5. Compared with the two groups of cells, migration and invasion were significantly enhanced (P <0.001). Conclusion: GPC3 eukaryotic expression vector can inhibit the proliferation of hepatocellular carcinoma cell line SK-Hep-1, decrease its adhesion to Matrigel and increase its migration and invasion ability. GPC3 may inhibit the proliferation of hepatocellular carcinoma cell line through inhibition of FGF2 signaling pathway.