导入野生型p53基因对T细胞淋巴瘤化疗敏感性的影响  

Effect of transfection of wild-type p53 gene on sensitivity of T cell lymphoma to chemotherapy

作　　者：吕方芳[1,2] 洪小南[1,2] 石必枝[3] 李宗海[3] 吴向华[1,2] 

机构地区：[1]复旦大学附属肿瘤医院肿瘤内科,上海200032 [2]复旦大学医学院肿瘤学系,上海200032 [3]上海市肿瘤研究所癌基因及相关基因国家重点实验室,上海200032

出　　处：《肿瘤》2009年第4期334-336,共3页Tumor

摘　　要：目的:探讨野生型p53基因对T细胞淋巴瘤Jurkat细胞化疗敏感性的影响。方法:用脂质体介导法,将p53基因导入Jurkat细胞,经G418筛选获得p53稳定表达的细胞,将细胞分别与0.1～100μg/mL阿霉素(doxorubicin,ADM)或0.1～100μg/mL足叶乙甙(etoposide,VP16)培养24h,采用MTT法检测细胞的生长抑制率。结果:转染p53基因的Jurkat细胞在0.47μg/mL ADM和2.5μg/mL VP16作用后,细胞生长抑制率为50%,与空载体转染组和未转染组比较,半数抑制浓度(halfinhibitory concentration,IC50)明显降低(P<0.05)。结论:p53基因能提高T细胞淋巴瘤Jurkat细胞对化疗药物ADM和VP16的敏感性,p53基因联合化疗药物可能成为耐药T细胞淋巴瘤治疗的新途径。Objective：To investigate the effect of exogenous wild type p53 gene transfection on the sensitivity of T lymphocytic lymphoma cell line Jurkat to chemotherapy. Methods： p53-gene was transfeeted into Jurkat cells by liposome mediation. Jurkat cells with stable expression of exogenous p53 gene were screened by G418. The cell viability was detected by trypan blue exclusion test. Then the cells were exposed to various concentrations of doxnrubiein（ ADM, 0.1-100.0 μg/ mL） and etoposide （VP16） for 24 h, and the cell viability was measured by MTT assay. Results：The inhibitory ratio on the proliferation of Jurkat cells with stable expression of exogenous p53 gene was 50% after treatment with 0.47 μg/mL ADM or 2.5 μg/mL VP16. Compared with the control cells transfeeted with empty vector or without any transfeetion, the value of half inhibitory concentration （ IC50 ） was significantly decreased （P 〈 0.05）. Conclusion：Expression of p53 could increase the sensitivity of T lymphoma Jnrkat cells to ADM and VP16. p53 gene combined with chemotherapy regimen mav become a novel approacb to treat drug-resistant T lymphoma.

关 键 词：淋巴瘤 T细胞 转染 基因 P53 细胞 JURKAT 

分 类 号：R733.73[医药卫生—肿瘤]