增加CIK细胞耐药性及杀瘤活性机制的研究  

Research on increasing multidrug resistance of Cytokine-induced killer (CIK) cells and mechanism of the anti-tumor activity

作　　者：师岩[1] 李淑艳[1] 王淑英[1] 吴琦[1] 张春晶[1] 髙涵 冯丽[1] 富东娜[1] 郭红艳[1] 齐晓丹[1] 

机构地区：[1]齐齐哈尔医学院生物化学教研室,161006

出　　处：《齐齐哈尔医学院学报》2010年第2期169-170,共2页Journal of Qiqihar Medical University

基　　金：黑龙江省教育厅科研基金项目(编号:11541406)

摘　　要：目的常规方法培养CIK细胞,将多药耐药基因(mdr1)转入细胞内,观察转染前后其对卡铂的耐药性及杀瘤活性机制进行研究。方法将mdr1的重组质粒转染到对数生长期的CIK细胞,通过RT-PCR鉴定耐药基因表达;Western blot检测mdr1编码的P-gp蛋白的表达;MTT法检测转染前后CIK细胞对卡铂敏感性的变化。结果在转染mdr1基因后的CIK细胞中,mdr1 mRNA阳性,P-gp的表达较转染前CIK细胞及转染空质粒的CIK细胞明显增高,差异有统计学意义(P<0.05),转染mdr1基因后的CIK细胞对卡铂的耐药性明显提高。结论mdr1基因转入CIK细胞后,细胞获得了对卡铂的耐药性。Objective To investigate the multidrug resistance to Carboplatin, the Cytokine--inducedkiller （CIK） cells transfeeted with the multidrug resistance（mdrl） e DNA. Methods CIK cells were induced by culturing PBMC with regular method. CIK cells were transfeeted with human mdrl cD- NA recombinant plasmid, RT--PCR was used to detect rndrl mRNA in transfeeted CIK cells. P--glycoprotein（P--gp） expression of CIK cells was assayed by western blotting. Multidrug resistance to Carboplatin were performed by MTT method. Results Mdrt mRNA was positive in transfected CIK cells, P--gp was higher expressed in the transfected CIK cells, as compared to those of untransfected CIK cells or CIK cells after transfection with empty plasmid, the multidrug resistance to Carboplatin increased （P 〈0.05）. Conclusions The successfully transfeeted with mdrl eDNA CIK cells bad the characteristics of multidrug resistance to Carbopltin.

关 键 词：细胞因子诱导的杀伤细胞 多药耐药 基因转染 

分 类 号：R730.51[医药卫生—肿瘤]