Liu Ning, Sun Li-guang, Yu Hui-ying, Zhang Yi, Yang Qing, Wang Xiao-peng
Division of Biochemistry & Molecular Biology, Shenyang Medical College, Shenyang 110034, China.
Zhonghua Zhong Liu Za Zhi. 2005 Apr;27(4):201-3.
To analyze the expression and functions of ERK (extracellular regulated kinase) in Fas-mediated apoptosis in gastric carcinoma cell line SGC-7901 and to elucidate the potential significance of this signaling pathway in tumor progression.
Radioisotope labeling and Western blotting with special anti-ERK antibody were used to check ERK activity in SGC-7901 cell line after anti-Fas antibody treatment. Apoptosis induced by several treatment factors was evaluated by FACS can flow cytometer.
ERK activity increased and reached the peak at 30 min after treatment with anti-Fas antibody and decreased in PD98059 pretreated group. The number of sub-G(1) cell was 30.5% +/- 2.6% in PD98059 pretreated group, which was higher than anti-Fas treatment group and control group, respectively.
In gastric cancer cell line SGC-7901, Fas-induced ERK activation may suppress Fas-mediated apoptosis. Inhibition of ERK may enhance the sensitivity of SGC-7901 cells to Fas-mediated apoptosis. Fas-induced ERK activation may confer gastric cancer cells ability to escape the immune surveillance.
分析细胞外调节激酶(ERK)在胃癌细胞系SGC-7901中Fas介导的凋亡中的表达及功能,阐明该信号通路在肿瘤进展中的潜在意义。
采用放射性同位素标记法及用抗ERK特异性抗体进行蛋白质印迹法检测抗Fas抗体处理后SGC-7901细胞系中的ERK活性。用流式细胞仪评估几种处理因素诱导的凋亡。
抗Fas抗体处理后ERK活性增强,在30分钟时达到峰值,而在PD98059预处理组中活性降低。PD98059预处理组中G1期前细胞数为30.5%±2.6%,分别高于抗Fas处理组和对照组。
在胃癌细胞系SGC-7901中,Fas诱导的ERK激活可能抑制Fas介导的凋亡。抑制ERK可能增强SGC-7901细胞对Fas介导凋亡的敏感性。Fas诱导的ERK激活可能赋予胃癌细胞逃避免疫监视的能力。