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目的 分析在胃癌细胞系SGC 790 1中,细胞外信号调节蛋白激酶(ERK)在Fas介导的信号通路中的表达及其作用,探讨该信号通路与胃癌发生和发展的关系。方法 利用同位素标记法和特异性识别磷酸化ERK抗体进行Western印迹杂交,检测Fas抗体孵育不同时间点胃癌细胞ERK的活性;利用流式细胞术检测胃癌细胞在各处理因素作用下细胞凋亡情况。结果 经抗Fas抗体处理后,胃癌细胞中ERK活性升高,在30min时达高峰;在MEK1抑制剂PD980 5 9作用下,ERK活性明显下降。抑制剂预处理组sub G1 细胞占30 .5 %±2 .6 %,单纯抗Fas抗体处理组sub G1 细胞占3.1 %±0 .2 %,对照组为3.0 %±0 .1 %。结论 在胃癌细胞中,抗Fas抗体可介导ERK活性的升高,导致细胞对Fas介导的凋亡信号脱敏;MEK1抑制剂可使胃癌细胞对Fas介导的凋亡信号敏感;胃癌细胞通过Fas介导的ERK的活化,逃逸免疫监视,持续生长。
Objective To investigate the expression of extracellular signal - regulated protein kinase (ERK) in Fas - mediated signaling pathway and its role in gastric cancer cell line SGC 790 1 to explore the relationship between this signaling pathway and the occurrence and development of gastric cancer. Methods The expression of ERK in gastric cancer cells was detected by radioimmunoassay (ELISA) and specific phospho-ERK antibody. The apoptosis of gastric cancer cells was detected by flow cytometry (FCM). Results After anti-Fas antibody treatment, the ERK activity in gastric cancer cells increased and peaked at 30 min. The ERK activity was significantly decreased by MEK1 inhibitor PD980 5 9. Sub G1 cells accounted for 30.5% ± 2.6% of the inhibitor pretreatment group, 3.1% ± 0.2% of the sub G1 cells in the anti-Fas antibody group, and 3.0% ± 0.1% of the control group. Conclusion In gastric cancer cells, anti-Fas antibody may mediate the increase of ERK activity, resulting in desensitization of cells to Fas-mediated apoptotic signaling; MEK1 inhibitor may sensitize gastric cancer cells to Fas-mediated apoptotic signaling; gastric cancer cells Fas-mediated activation of ERK escapes immune surveillance and continues to grow.