肝细胞癌中BTG2基因的表达及其对肝细胞癌细胞增殖和凋亡影响的研究

Expression of BTG2 gene in hepatocellular carcinoma and the influence to proliferation and apoptosis in HepG2 cell

关键词:  肝细胞癌  BTG2基因  HepG2细胞  增殖  凋亡

Key words:  [Key words]　human hepatocellular carcinoma  BTG2 gene  HepG2 cell  proliferation  apoptosis

摘要:

目的　研究肝细胞癌中BTG2基因的表达以及BTG2基因对肝细胞癌HepG2细胞增殖和凋亡的影响。　方法　　荧光定量PCR测定47例肝细胞癌组织中BTG2基因的表达情况。构建表达载体pcDNA-BTG2，转染HepG2细胞。转染后，蛋白质印迹法检测转染后BTG2蛋白的表达，MTT法测定细胞生长抑制率，双标流式细胞法检测细胞凋亡率。　结果　　与癌旁组织相比，BTG2 mRNA在肝细胞癌组织中表达明显下调（P<0.01）。且BTG2的表达与肝细胞癌的分级相关，随着分化程度的升高呈逐渐增加的趋势，但与肝细胞癌的分期及淋巴结转移、远处转移无关。转染表达载体pcDNA-BTG2能够显著上调HepG2细胞中BTG2蛋白的表达，同时，细胞生长抑制率及凋亡率明显增加（P<0.01）。　结论　　在肝细胞癌中BTG2基因表达下调，其表达上调能够抑制肝癌细胞增殖并促进凋亡。

Abstract:

[Abstract] Objective　To study the expression of BTG2 gene in hepatocellular carcinoma and the influence of BTG2 gene to proliferation and apoptosis in HepG2 cells. 　Methods　The expression of BTG2 gene in 47 cases of hepatocellular carcinoma was detected with real-time PCR. The expression vector pcDNA3.3-BTG2 was constructed and transfected to HepG2 cells. Then, the expression of BTG2 protein was detected by western blot, and the growth inhibitory rate and apoptosis rate of the transfected cells was detected by MTT experiment and flow cytometry. 　Results　The expression of BTG2 gene presented an obvious decreasing in hepatocellular carcinoma. And the expression of BTG2 was related with the classification of hepatocellular carcinoma, with increasing of differentiation there was a gradually increasing trend. But it was not related with the staging, lymph node metastasis and distant metastasis of hepatocellular carcinoma. After transfecting with pcDNA3.3-BTG2, the expression of BTG2 protein of the transfected HEPG2 cells up-regulated significantly. Comparing to the control cells, the apoptosis of experimental group cells increased significantly(P<0.01). 　Conclusion　There is the expression decreasing of BTG2 gene in hepatocellular carcinoma. The over-expression of BTG2 gene can inhibit proliferation and increase apoptosis of HepG2 cells.