目的　探讨EB病毒潜伏膜蛋白 1(LMP1)是否通过NF κB在鼻咽癌细胞中促进p5 3蛋白的表达 ,为阐明LMP1促进细胞凋亡的机制提供实验依据。方法　利用四环素诱导表达系统 ,建立受四环素调控表达LMP1的鼻咽癌细胞系。用报道基因检测法和Western印迹技术 ,观察LMP1过量表达对NF κB的功能性活化及p5 3、bcl 2表达的影响。结果　在鼻咽癌细胞中 ,LMP1能活化NF κB。过量表达的LMP1促进p5 3基因的表达 ,这种促表达可以被硫代磷酸化修饰的LMP1及p6 5反义寡聚脱氧核苷酸阻断。LMP1和p6 5对bcl 2的表达则没有影响 ,LMP1过表达对bcl 2的表达无影响。结论鼻咽癌中LMP1通过活化核转录因子NF κB调节p5 3的表达 ;而在LMP1过表达时 ,bcl 2介导的抗凋亡机制未被启动 ,至少是未被上调的。 Objective To investigate whether Epstein-Barr virus latent membrane protein 1 (LMP1) promotes the expression of p5 3 protein in nasopharyngeal carcinoma cells through NF κB, and provide an experimental basis for elucidating the mechanism of LMP1 promoting apoptosis. Methods Tetracycline-inducible expression system was used to establish a cell line of nasopharyngeal carcinoma which was controlled by tetracycline and expressed LMP1. The effects of LMP1 overexpression on the functional activation of NF κB and the expression of p5 3 and bcl 2 were observed by reporter gene assay and Western blotting. Results In NPC cells, LMP1 activates NF-κB. Overexpression of LMP1 promotes the expression of the p5 3 gene, which can be blocked by thiophosphorylation of LMP1 and p6 5 antisense oligodeoxynucleotides. LMP1 and p6 5 had no effect on the expression of bcl 2, while LMP1 overexpression had no effect on the expression of bcl 2. Conclusion LMP1 regulates the expression of p5 3 by activating NF-κB in NPC. However, the anti-apoptotic mechanism mediated by bcl 2 is not activated or at least not up-regulated when LMP1 is overexpressed.