摘要
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 investigatethe relationship between p38 MAPK pathway and multidrug resistance of stomach cancer. The activity of p38 MAP kinase in stomach cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR were examined by immunoprecipition after adriamycin treatment SGC7901 for 0, 2, 15, 30 and SGC7901/VCR for 0, 2, 15, 30, 60 minutes,respectively. The results indicated that adriamycin could activate the activity of p38 MAP kinase in gastric cancer cell SGC7901 with time dependency, but could decrease remarkably the activity of p38 MAP kinase in gastric cancer multidrug resistant cell SGC7901/VCR after adriamycin treatment it for 15 minutes. It suggested that adriamycin could affect the activity of p38 MAPK in gastric cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2001年第1期24-26,共3页
Medical Journal of Chinese People's Liberation Army
基金
国家自然科学基金!(编号 39470 785)
全军医药卫生青年基金!(编号 96Q0 78)
