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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: To study the effect of GPC3 eukaryotic expression vector on the biological behavior of hepatoma cells. Methods: The EGFP-N2-GPC3 enhanced green fluorescent protein expression vector was transfected into SK-Hep-1 human hepatocellular carcinoma cells by lipofectamine. After the GPC3 cells were successfully transfected into the cells, the proliferation, adhesion, Exercise and in vitro invasiveness. The effects of four growth factors, FGF2, IGF2, BMP4 and TGFβ1, on GPC3 cell proliferation were also observed. Results: GPC3 could inhibit the proliferation of SK-Hep-1, decrease the adhesion to Matrigel and increase the migration and invasion ability of SK-Hep-1. GPC3 could inhibit the proliferation of SK-Hep- The growth factors IGF2, BMP4, TGFβ1 no such effect. Conclusion: GPC3 eukaryotic expression vector can inhibit the proliferation of SK-Hep-1 hepatoma cells, but it can reduce its adhesion to Matrigel and increase its migration and invasion ability. GPC3 may inhibit FGF2 signaling pathway to inhibit the proliferation of hepatoma cells proliferation.