摘要
目的初步探讨核转录因子NF-κB在TRAIL诱导肝癌细胞发生凋亡过程中的作用和可能机制。方法应用流式细胞仪技术检测经TRAIL和(或)MG-132处理后,肝癌细胞SMMC-7721凋亡发生情况;采用蛋白印渍技术检测TRAIL处理后SMMC-7721细胞凋亡相关蛋白表达情况;并用ELISA法检测NF-κB活性变化。结果单独使用TRAIL后,肝癌细胞发生凋亡,其凋亡指数为15．1％;若联合应用NF-κB抑制剂-MG-132后,则凋亡指数达27．4％,明显高于前者(P<0．01);同时,两者均高于对照组(P<0．01)。SMMC-7721细胞经TRAIL处理后,抗凋亡蛋白表达增加,而促凋亡蛋白表达下降。另外,经TRAIL单独处理后,细胞的NF-κB活性(0．49±0．02)明显高于其余各组(P<0．01)。结论NF-κB在TRAIL诱导的肝癌细胞凋亡过程中被激活,而NF-κB又可能通过促进抗凋亡蛋白的表达、抑制促凋亡蛋白的表达,从而抑制肿瘤细胞的凋亡。
Objective To investigate the role of NF-κB in induction of apoptosis of hepatocellular carcinoma cells with TRAIL. Methods Cell apoptosis, activity of NF-κB, expression of apoptosisrelated proteins in SMMC-7721 cells treated with TRAIL and/or MG-132 were determined with flow cytometry, ELISA and Western blot. Resdts The cell apoptosis index was significantly lower in TRAIL group than in the group of TRAIL with MG-132 treatment （15.1% vs. 27.4%, P〈0. 01）. However, it was higher in the 2 groups than in the control （P〈0.01）. SMMC-7721 cells overexpressed anti-apoptosis proteins, while down-regulated the expression of pro-apoptosis protein after receiving the treatment of TRAIL. In addition, the activity of NF-κB significantly increased in the TRAIL group as compared with the other 2 groups （P〈0. 01）. Conclusions NF-κB plays an important role of anti-apoptosis effect on the course of apoptosis induction by TRAIL. Therdore, NF-κB inhibitors can inhibit the growth of tumor if being used properly or in combination with other chemotherapeutic drugs.
出处
《中华肝胆外科杂志》
CAS
CSCD
2006年第12期850-852,共3页
Chinese Journal of Hepatobiliary Surgery
