AS-mCLB1重组质粒联合多西紫杉醇抗Lewis肺癌细胞增殖活性的研究  

The enhancement of the recombinant plasmid pAS-mCLB1 to Docetaxel on inhibiting proliferation of Lewis lung carcinoma cells

作　　者：张涛[1] 张伶[1] 魏东[1] 张汝[1] 程朋[1] 

机构地区：[1]中国人民解放军成都军区总医院肿瘤科,成都610083

出　　处：《四川大学学报（自然科学版）》2008年第3期703-708,共6页Journal of Sichuan University(Natural Science Edition)

基　　金：浙江省博士后科研项目择优资助资金(2006-bsh-34);浙江省自然科学基金(Y207353)

摘　　要：pAS-mCLB1转染Lewis肺癌(LL/2)细胞72 h后,再加用多西紫杉醇(40 nmol/L)处理细胞,MTT法测定药物对LL/2细胞的体外杀伤作用.另将LL/2细胞接种C57BL/6小鼠,成瘤后分别用pAS-mCLB1、多西紫杉醇和pAS-mCLB1+多西紫杉醇处理动物,3天1次,共4次,观察肿瘤体内增殖情况,流式细胞仪检测动物肿瘤组织的细胞凋亡.结果显示:pAS-mCLB1联合多西紫杉醇可明显降低LL/2细胞体内、外增殖活性,同时促使肿瘤组织中细胞凋亡增加,两种方法具有协同作用.pAS-mCLB1显著增强多西紫杉醇抗肿瘤效应,此增强作用可能与pAS-mCLB1诱导肿瘤细胞凋亡,提高了多西紫杉醇的细胞毒作用有关.After transfected with pAS-mCLB1 through Lipofectamine 2000, Lewis lung carcinoma （LL/2） cells were treated with Docetaxel （40 nmol/L） in vitro. The cytotoxicity of Docetaxel to LL/2 cells was measured by MTT assay. To further test the efficacy of pAS-mCLB1 in vivo, LL/2 cells were implanted into C57BL/6 mice. When tumors developed, LL/2-loaded mice were treated with pAS-mCLB1 plus Docetaxel once every three days for four times. Tumorigenicity was observed and apoptosis of cells in tumor tissues was determined by flow cytometry. Cytotoxicity of Docetaxel to LL/2 cells which were transfected with pASmCLB1 was more obvious than controls. For in vivo testing, tumorigenicity was inhibited, cell apoptosis induced evidently in the group of pAS-CLB1 combined with Docetaxel. pAS-mCLB1 slightly increased the effect of Docetaxel on inhibiting proliferation of LL/2 cells in vitro and in vivo. This function may be associated with the ability of pAS-mCLB1 to enhance the anti-tumor activity of Docetaxel by inducing cell apoptosis.

关 键 词：细胞周期蛋白B1 反义CDNA 重组质粒 多西紫杉醇 凋亡 

分 类 号：Q291[生物学—细胞生物学]