紫杉醇在人胃癌细胞系SGC-7901中的抗肿瘤作用  

Paclitaxel exert anti-cancer bioactivity on SGC-7901 cell by inhibiting expression of p-mTOR

作　　者：孙东[1] 靖昌庆[1] 郭晓波[1] 李乐平[1] 

机构地区：[1]山东大学附属省立医院胃肠外科,山东济南250021

出　　处：《中国现代普通外科进展》2016年第3期169-174,共6页Chinese Journal of Current Advances in General Surgery

基　　金：山东省自然科学基金面上项目(ZR2011HM041)

摘　　要：目的:探讨紫杉醇对人胃癌细胞系SG C-7901增殖、迁移、凋亡及细胞周期的影响并探究其可能的作用机制。方法:根据培养基中紫杉醇的浓度将实验分为三组即对照组、0.25μg/m L组、0.5μg/m L组;C C K-8和克隆形成实验检测细胞活性,Transw ell实验观察细胞的迁移及侵袭能力,流式细胞术检测细胞凋亡及周期变化,W estern blot分析m TOR及p-m TOR蛋白表达变化。结果:C C K-8及克隆形成结果表明紫杉醇可以降低SG C-7901的细胞活性,Transw ell结果证明紫杉醇可以抑制SG C-7901的迁移及侵袭能力,流式细胞术分析显示紫杉醇可以诱导细胞凋亡,各实验组凋亡率分别为(6.77±0.51)%、(10.53±0.91)%、(13.97±1.92)%;细胞周期结果证实紫杉醇可使细胞周期阻滞于G_2/M期,各实验组G_2/M期比例分别为(10.81±1.23)%、(14.57±1.78)%、(15.54±2.17)%;W estern blot结果证实紫杉醇还可以降低p-m TOR蛋白的表达,差异均具有统计学意义(P<0.05)。结论:紫杉醇可以通过下调p-m TOR的表达抑制人胃癌细胞系SG C-7901的细胞活性并诱导其凋亡,可能是其抗肿瘤作用的分子学机制。Objective： To investigate the effects of paclitaxel exerted on gastric cancer cells SGC-7901 and further explore the potential mechanism. Methods： SGC-7901 cells were randomly divided into three groups： control group, 0.25μg/m L group and 0.5μg/m L group according to the concentration of paclitaxel in the medium. CCK-8 and colony formation were employed to test cell viability, Transwell was used to analysis cell invasion ability, cell cycle and apoptosis were tested by flow cytometry, the expression of m TOR and p-m TOR protein were measured by Western blot. Results：CCK-8 and colony formation results demonstrated paclitaxel could inhibit cell viability, transwell results showed cell invasion ability could be attenuated by paclitaxel, flow cytometry results confirmed paclitaxel induced cell apoptosis and arrested cell cycle at G2/M phase. The expression of p-m TOR protein was decreased in paclitaxel-treated cells. Both results were statistical significantly（P〈0.05）.Conclusion： Paclitaxel can exert anti-cancer bio-activity on SGC-7901 cell by inhibiting the expression of p-m TOR.

关 键 词：紫杉醇 SGC-7901细胞 MTOR信号通路 

分 类 号：R735.2[医药卫生—肿瘤]