转染反义DcR3真核表达载体协同氟尿嘧啶诱导肝癌细胞凋亡  

Induction of HCC cell apoptosis by antisense DcR3 and 5-fluorouracil

作　　者：段伟宏[1] 苏忠学[2] 吴泰璜[2] 

机构地区：[1]山西省肿瘤医院普外科,太原市030013 [2]山东大学省立医院,济南市250012

出　　处：《中华肝胆外科杂志》2006年第2期98-100,共3页Chinese Journal of Hepatobiliary Surgery

摘　　要：目的研究 DcR3反义 mRNA 与氟尿嘧啶对肝癌细胞的影响。方法用 MTT、TUNEL、流式细胞术分别检测反义重组体组、氟尿嘧啶处理组、协同作用组对肝癌细胞株SMMC7721的影响。结果协同作用组促凋亡作用明显强于其余二组。结论 PVAX Ⅰ-as-DcR3与氟尿嘧啶协同作用可使在氟尿嘧啶浓度降低的同时保持较强的促肝癌细胞凋亡作用。Objective To study the apoptosis of HCC cells induced by PVAX Ⅰ-as-DcR3 and 5 Flu. Methods MTT, TUNEL and FCM were used to determine and compare the apoptosis of HCC cells induced by simple PVAX Ⅰ-as-DcR3 （group A）, simple 5-Flu （group B） and PVAX Ⅰ-as-DcR3 in combination with 5-Flu （group C）. Results The inducing effects were significantly higher in group C than in other 2 groups. Conclusions PVAX Ⅰ-as-DcR3 in combination with 5-Flu has a strong indu cing effect on HCC cells in low concentration of 5-Flu.

关 键 词：癌 肝细胞 反义 转染 表达载体 凋亡 

分 类 号：R735.7[医药卫生—肿瘤] R979.1[医药卫生—临床医学]