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[细胞外信号调节激酶对人胃癌细胞Fas介导的凋亡信号通路的作用]

[The function of ERK on Fas-mediated apoptotic signaling pathway of human gastric carcinoma cells].

作者信息

Liu Ning, Sun Li-guang, Yu Hui-ying, Zhang Yi, Yang Qing, Wang Xiao-peng

机构信息

Division of Biochemistry & Molecular Biology, Shenyang Medical College, Shenyang 110034, China.

出版信息

Zhonghua Zhong Liu Za Zhi. 2005 Apr;27(4):201-3.

Abstract

OBJECTIVE

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.

METHODS

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.

RESULTS

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.

CONCLUSION

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.

摘要

目的

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。

方法

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。

结果

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。

结论

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。

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