抑制PI3K/Akt信号通路提高膀胱癌化疗效果的实验研究  

Inhibition of PI3K/Akt signal pathway improves chemotherapeutic effect of bladder cancer

作　　者：董自强[1] 江克华[1] 宋兴福[1] 陈先国[2] 陈晓波[1] 袁红纲[1] 刘幼昆[1] 龙兵[1] 

机构地区：[1]三峡大学第一临床医学院泌尿外科,湖北省宜昌市443003 [2]武汉大学人民医院泌尿外科,430060

出　　处：《实用医学杂志》2012年第2期181-183,共3页The Journal of Practical Medicine

基　　金：三峡大学硕士学位论文培优基金项目(编号:2011PY031);三峡大学研究生科研创新基金项目(编号:2010CX052)

摘　　要：目的:探讨通过抑制Akt信号通路提高抗癌药物紫杉醇对膀胱癌T-24的杀伤作用。方法:采用MTT法检测Akt抑制剂鱼藤素、紫杉醇单独以及两药联合应用对T-24细胞的增殖抑制率,采用流式细胞术(FCM)检测药物单独或联合作用对细胞周期的影响。结果:联合鱼藤素能够显著提高紫杉醇对T-24细胞的增殖抑制率(P<0.01),协同治疗指数<1,具有协同治疗作用;FCM结果显示联合鱼藤素使细胞阻滞在G0/G1期的比例增加,S期比例减少,与对照组比较,差异有统计学意义(P<0.05)。结论:抑制Akt信号通路能够显著提高紫杉醇对膀胱癌T-24细胞的杀伤作用。Objective To explore whether the inhibition of PI3K/Akt signal pathway increases the tumor- killing effects of anticancer drugs paclitaxel on bladder cancer T-24 cells. Methods The inhibitory rate of T-24 cells were observed by MTF assay after treatment with different concentrations of individual Akt inhibitor deguelin, paclitaxel, and deguelin plus paclitaxel, and their cell cycle were detected by flow eytometry. Results The inhibition ratio of proliferation of T-24 cells was increased significantly by Paelitaxel in combination with deguelin （P 〈 0.01 ）. deguelin had synergistic effects with Paelitaxel （combination index 〈 1）; Flow cytometry showed that deguelin and Paclitaxel blocked the cell cycle mainly in the G0/G1 stage, while the combined medication lengthen the G0/G1 phase and shorten the S phase compared with individual deguelin or Paclitaxel. Conclusion The tumor-killing effect of Paclitaxel on T-24 cells was increased significantly by inhibition of PI3K/Akt signal transduction pathway,

关 键 词：药物协同作用 鱼藤素 P13K/AKT T-24细胞 

分 类 号：R737.14[医药卫生—肿瘤]