胆囊癌细胞对吉西他滨化疗敏感性的试验研究  

Experimental study on the sensitivity of gallbladder cancer cells to Gemcitabine chemotherapy

作　　者：徐明[1] 沈火剑[1] 朱宏毅[1] 李可为[1] 王坚[1] 施维锦[1] 季福[1] 

机构地区：[1]上海交通大学医学院附属仁济医院胆胰外科,上海200127

出　　处：《肝胆胰外科杂志》2015年第4期303-307,共5页Journal of Hepatopancreatobiliary Surgery

摘　　要：目的探寻胆囊癌细胞对吉西他滨化疗敏感的潜在分子标记物。方法将两株对吉西他滨敏感性具有较大差异的胆囊癌细胞进行DNA微阵列检测,并进行精巧传导通路分析(IPA),最后采用免疫荧光定量PCR与蛋白印迹实验进一步验证。结果通过对吉西他滨敏感性截然相反的两株胆囊癌细胞进行DNA微阵列分析,发现表达水平差值在4倍以上的基因有633个,其中PI3K/AKT信号在SGC-996细胞株中处于抑制状态,但其下游信号p70S6K处于激活状态;对有差异的16个基因进行RT-PCR检测,与DNA微阵列检测相比,基因表达趋势基本一致;RT-PCR与蛋白印迹实验表明AKT/ERK信号通路在对吉西他滨不敏感的胆囊癌细胞中处于抑制状态,与精巧传导通路分析结果一致。结论对吉西他滨敏感性不同的胆囊癌细胞系GBC-SD与SGC-996之间存在着基因表达差异,其中AKT/ERK等可能作为胆囊癌对吉西他滨敏感的预测指标。Objective To explore the potential markers that is sensitive for gallbladder carcinoma cells to Gemcitabine（Gem）.Methods Two GBC cell lines with vast difference in sensitivity to Gem were subjected to DNA microarray analysis.The results were again analyzed by Ingenuity Pathway Analysis（IPA） and further verified by Real-time Quantitative PCR and Western blotting experiments.Results DNA microarray analysis showed that there were 633 genes which the expression level was more than 4 times,in which PI3K/AKT signal pathway in SGC-996 cell line was not activated,but the downstream signal p70S6 K is in the activated state.The results of DNA microarray analysis and RT-PCR for 16 different genes showed almost the same gene expression trend.AKT/ERK signal pathway was in the inhibitory state in SGC-996 cell,RT-PCR and Western blotting experiment verified the reliability of the forecast results of IPA.Conclusion There is gene expression difference between gallbladder carcinoma cell lines GBC-SD and SGC-996 which is different sensitive to Gem.AKT/ERK may be used as predictive marker for gallbladder cancer sensitive to Gem.

关 键 词：胆囊癌 化疗 敏感性 

分 类 号：R735.8[医药卫生—肿瘤]