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研究 p38MAPK信号转导途径在胃癌耐药机制中的意义。用免疫共沉淀法及Westernboltting实验分别研究阿霉素处理胃癌细胞SGC790 1及胃癌多药耐药SGC790 1/VCR细胞后 ,p38激酶活性及量的变化。结果显示 ,阿霉素处理胃癌多药耐药SGC790 1/VCR细胞 15min后 ,p38MAPK活性明显降低 ,且发现 p38MAPK量也明显下降。与之不同 ,阿霉素处理SGC790 1细胞后 ,p38MAPK活性增强 ,呈时间依赖性 ,而 p38MAPK量无明显变化。提示肿瘤化疗药物阿霉素可诱导肿瘤耐药细胞 p38激酶活性降低 ,且可诱导非耐药细胞p38激酶活性增强。
To study the significance of p38MAPK signal transduction pathway in gastric cancer drug resistance. The co-immunoprecipitation and Western bolttting experiments were used to study the changes of p38 kinase activity and quantity after treatment with adriamycin in gastric cancer cells SGC790 1 and gastric cancer multidrug resistant SGC790 1/VCR cells. The results showed that after treatment with doxorubicin for multidrug resistant SGC790 1/VCR cells for 15 min, p38MAPK activity was significantly reduced, and the amount of p38MAPK was also found to be significantly decreased. In contrast, p38MAPK activity was enhanced after doxorubicin treatment of SGC790 1 cells in a time-dependent manner, whereas the amount of p38MAPK did not change significantly. It was suggested that adriamycin, a tumor chemotherapeutic drug, could induce the decrease of p38 kinase activity in tumor-resistant cells and induce the increase of p38 kinase activity in non-drug resistant cells.