摘要
目的探讨生长抑素（SST）逆转胆囊癌细胞株耐药性的作用机制。方法将胆囊癌细胞株（GBC-SD）分为4组：单独SST作用组、单独阿霉素作用组、联合用药组（SST预处理24h后，再加入阿霉素）和对照组。药物作用24、48、72和96h时，采用MTT法观察各组细胞生长曲线。同时，运用Western blot方法检测SST作用后GBC-SD细胞内ICBP90和拓扑异构酶α（Topo Ⅱ α）的蛋白表达的情况。结果单独应用SST对GBC-SD细胞没有明显的生长抑制作用（P〉0．05）；而SST作用于GBC-SD细胞24h时，ICBP90和Topo Ⅱ α蛋白的表达都明显增多（P〈0．05）。结论生长抑素可能是通过上调ICBP90的表达来增加Topo Ⅱ α的表达，从而增强阿霉素的杀伤作用。
Objective To investigate the mechanism of increasing chemosensitivity of gallbladder carcinoma stimulated by somatostatin. Methods GBC-SD cells were divided into four groups： SST-alonetreated group, Doxorubicin （DOX） -alone-treated group and co-treated group （co-treatment of SST and DOX）. In the control group,the cells were cultivated by medium only. In SST-alone-treated group,the cells were cultivated by medium with SST in the concentration of 75 μg/ml. In DOX-alone-treated group,the cells were cultivated by medium with DOX in the gradient concentrations of 5,10,20 μg/ml. In the co-treated group,cells were first cultivated by medium with 75 μg/ml SST for 24 h, followed by the addition of DOX in the gradient concentrations mentioned above. Cell viability curve was measured by MTT assay at 24,48,72 and 96 h, respectively. Meanwhile, the alterations of protein expressions of ICBP90 and Topo Ⅱ α after treatment of SST were examined by Western blot. Results The treatment of SST alone on GBC-SD cells did not exert significantly inhibitory effect compared to the control group （ P 〉 0. 05 ）. However, 24 h after the treatment of SST, the protein expressions of ICBP90 and Topo Ⅱ α were both up-regnlated （ P 〈 0. 05 ）. Conclusion Up-regulated the expression of ICBP90 by somatostatin maybe the cause of overexpression of Topo Ⅱ α,which leads to the enhanced lethal effect of DOX.
出处
《中华外科杂志》
CAS
CSCD
北大核心
2008年第5期381-383,共3页
Chinese Journal of Surgery
基金
国家自然科学基金资助项目（30571824）
关键词
胆囊肿瘤
生长抑素
基因研究
Gallbladder neoplasms
Somatostatin
Gene research
