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目的 研究 p38分裂原激活蛋白激酶 (MAPK)信号转导途径在胃癌耐药形成中的意义。方法 用免疫共沉淀法及Westernbolt法分别研究长春新碱处理胃癌细胞SGC790 1及胃癌多药耐药SGC790 1/VCR细胞内 p38MAPK活性及量的变化。 结果 胃癌多药耐药SGC790 1/VCR细胞及亲本SGC790 1细胞内均存在活性 p38MAPK ,长春新碱处理此两种细胞均可引起 p38MAPK活性增强 ,后者反应迅速 ,可在 2min内刺激p38MAPK活性增高 ,而前者反应较慢 ,至 30min时才观察到 p38MAPK活性增高。结论 p38MAPK信号转导途径可能与长春新碱的抗肿瘤活性相关 ,肿瘤细胞内 p38MAPK对长春新碱刺激的反应速度可能与胃癌长春新碱耐药相关
Objective To study the significance of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the drug resistance of gastric cancer. Methods Immunoprecipitation and Western blot were used to study the changes of p38MAPK activity and the amount of vincristine in gastric cancer cell line SGC790 1 and gastric cancer multidrugresistant SGC790 1 / VCR cell line, respectively. Results Both p38MAPK and p38MAPK were present in SGC790 1 / VCR cells and parental SGC7901 cells. Vincristine treatment of both cells induced p38MAPK activity, which was rapidly responded to, which stimulated p38MAPK activity in 2min , While the former response is slow, to 30min was observed p38MAPK activity increased. Conclusion The p38MAPK signal transduction pathway may be related to the anti-tumor activity of vincristine. The response rate of p38MAPK to vincristine stimulation in tumor cells may be related to vincristine resistance in gastric cancer