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目的探讨B7-H1(B7-homolog 1)在乙型肝炎病毒(HBV)感染导致的肝细胞癌(HCC)中的作用机制。方法通过慢病毒lentivirus-B7-H1转染人正常肝细胞系L02、人肝癌细胞系HepG2、HepG2.2.15后,应用MTT法观察细胞活性,流式细胞仪检测细胞的凋亡情况,Western blot技术检测蛋白B7-H1、Survivin蛋白的变化情况。结果抑制B7-H1表达水平后,通过MTT检测表明细胞系HepG2.2.15细胞活性比HepG2细胞、L02细胞活性降低,流式细胞仪检测凋亡增加,同时Western blot显示Survivin蛋白的表达减少。结论通过慢病毒转染抑制B7-H1的表达可以促进细胞系HepG2.2.15凋亡,B7-H1可能是通过调控Survivin的变化影响HBV感染的肿瘤细胞的增殖与凋亡。
Objective To investigate the mechanism of B7-homolog 1 in hepatocellular carcinoma (HCC) caused by Hepatitis B virus (HBV) infection. Methods Human leukemia cell lines L02 and HepG2.2.15 were transfected with lentivirus-B7-H1 lentivirus-B7-H1, and the cell viability was observed by MTT assay. The apoptosis of cells was detected by flow cytometry and Western blot Detection of protein B7-H1, Survivin protein changes. Results After inhibiting the expression of B7-H1, the activity of HepG2.2.15 cells was lower than that of HepG2 cells and L02 cells by MTT assay. The apoptosis of HepG2.2.15 cells was detected by flow cytometry, and the expression of Survivin protein was decreased by Western blot. Conclusion Inhibition of B7-H1 expression by lentiviral transfection can promote the apoptosis of HepG2.2.15 cells. B7-H1 may affect the proliferation and apoptosis of HBV-infected tumor cells through the regulation of Survivin.