GATA4在肝癌细胞中的表达及其对肝癌细胞增殖、迁移和侵袭能力的影响

Expression of GATA4in hepatocellular carcinoma cells and its effect on proliferation,migration and invasion of hepatocellular carcinoma cells

目的探索转录因子GATA4在肝癌细胞系中的表达及其表达改变对肝癌细胞增殖、迁移和侵袭能力的影响。方法通过RT-PCR和Western Blot检测正常肝细胞、肝癌细胞系的表达,在体外构建GATA4基因沉默和过表达模型,分析并比较转录因子GATA4表达变化对肝癌细胞增殖、迁移和侵袭的影响。结果GATA4mRNA在肝癌细胞系(SMMC7721、Hep3B)中高表达,在正常肝细胞HLLP-7702和HepG2中低表达,GATA4蛋白在正常肝细胞(HL-7702)和肝癌细胞系(SMMC7721、Hep3B和HepG2)中均低表达;GATA4高表达抑制肝癌细胞(HepG2)增殖、迁移和侵袭(P<0.05),GATA低表达促进肝癌细胞(Hep3B)增殖、迁移和侵袭(P<0.05)。结论GATA4mRNA在部分肝癌细胞系中高表达,GATA4蛋白质水平在肝癌细胞系和正常肝细胞中均低表达。上调GATA4表达水平可显著抑制肝癌细胞(HepG2)增殖、迁移和侵袭能力,相反,下调GATA4的表达水平增强肝癌细胞(Hep3B)的增殖、迁移和侵袭能力,确切机制有待进一步探讨。

Objective To investigate the expression of transcription factor GATA4in hepatocellular carcinoma(HCC)cell lines and its effect on the proliferation,migration and invasion of HCC cell lines.Methods RT-PCR and Western Blot were used to detect the expression of normal hepatocyte and HCC cell lines.The GATA4gene silencing and overexpression model was constructed in vitro.The effects of GATA4expression changes on proliferation,migration and invasion of HCC cell lines were analyzed and compared.Results GATA4mRNA was highly expressed in HCC cell lines(SMMC7721,Hep3B),low expression in normal hepatocyte(HLLP-7702)and HCC cell line(HepG2);GATA4protein was downregulated in both normal hepatocytes(HL-7702)and HCC cell lines(SMMC7721,Hep3 Band Hep G2).Overexpression of GATA4inhibited HCC cell(HepG2)proliferation,migration and invasion(P<0.05),and low expression of GATA promoted HCC cell(Hep3B)proliferation,migration and invasion(P<0.05).Conclusion GATA4mRNA is highly expressed in some HCC cell lines,and GATA4protein was downregulated in both normal hepatocytes(HL-7702)and HCC cell lines(SMMC7721,Hep3 Band HepG2).Up-regulation of GATA4expression can significantly inhibit the proliferation,migration and invasion of HCC cell(HepG2).Conversely,down-regulation of GATA4 expression enhances the proliferation,migration and invasion of HCC cell(Hep3B).The exact mechanism of needs to be further explored.