JNK/c-Jun信号通路参与介导EB病毒编码的BARF1基因上调胃癌细胞Bcl-2的表达

JNK/c-Jun signaling pathway contributes to mediate Epstein-Barr virus-encoded BARF1 gene up-regulating Bcl-2 expression in human gastric carcinoma cells

目的:探讨EB病毒编码的BARF1基因对胃癌细胞JNK-MAPK信号通路活性及Bcl-2基因表达的影响。方法:以p SG5空载体转染的胃癌细胞系BGC823(BGC-SG)为对照,采用蛋白质印迹分析稳定表达BARF1的BGC823细胞(BGC-BARF1)中,以及采用JNK-MAPK的特异性抑制剂SP600125处理后JNK和c-Jun蛋白的磷酸化水平以及cJun和Bcl-2蛋白的表达。结果:与BGC-SG相比,BGC-BARF1细胞中JNK和c-Jun蛋白的磷酸化水平,以及c-Jun和Bcl-2蛋白的表达均显著提高(P<0.05)。SP600125处理后,c-Jun蛋白的磷酸化水平以及c-Jun和Bcl-2蛋白的表达均显著下降。结论:JNK/c-Jun信号通路参与介导BARF1上调胃癌细胞中Bcl-2的表达。

Objective: To investigate the effect of the JNK/c-Jun signaling pathway on mediating Epstein-Barr virus-encoded BARF1 gene up-regulating Bcl-2 expression in human gastric carcinoma cells.Methods: Western blotting was performed to analyze the levels of JNK and c-Jun protein phosphorylations and of the total c-Jun and Bcl-2 protein expressions in BARF1-stably-expressing human gastric carcinoma cell line BGC823( BGC-BARF1) under the control of p SG5 vector transfected one( BGC-SG). Results:The levels of the JNK and c-Jun protein phosphorylations,and of the c-Jun and Bcl-2 protein expressions were significantly increased in BGC-BARF1 compared with the BGC-SG controls,and blocked by special inhibitor of JNK-MAPK SP600125( all P < 0. 05). Conclusion: JNK / c-Jun signaling pathway contributes to mediate BARF1 gene up-regulating the Bcl-2 expression in human gastric carcinoma cells.