CAJ | 학술논문

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p53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p53、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p53基因的表达，这种促表达可以被硫代磷酸化修饰的LMP1及p65反义寡聚脱氧核苷酸阻断。LMP1和p65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p53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。
목적탐토EB병독잠복막단백1（LMP1）시부통과NF-κB재비인암세포중촉진p53단백적표체，위천명LMP1촉진세포조망적궤제제공실험의거。방법이용사배소유도표체계통，건립수사배소조공표체LMP1적비인암세포계。용보도기인검측법화Western인적기술，관찰LMP1과량표체대NF-κB적공능성활화급p53、bcl-2표체적영향。결과재비인암세포중，LMP1능활화NF-κB。과량표체적LMP1촉진p53기인적표체，저충촉표체가이피류대린산화수식적LMP1급p65반의과취탈양핵감산조단。LMP1화p65대bcl-2적표체칙몰유영향，LMP1과표체대bcl-2적표체무영향。결론비인암중LMP1통과활화핵전록인자NF-κB조절p53적표체；이재LMP1과표체시， bcl-2개도적항조망궤제미피계동，지소시미피상조적。
Objective　To ascertain if EBV- encoded latent membrane protein 1 (LMP1) induces p53 expression via NF-κB signaling.Methods　A nasopharyngeal carcinoma cell line, Tet-on-LMP1 HNE2, transfected with LMP1,the expression of which was regulated by tetracycline, was used in this study. Functional activity of NF-κB was determined by luciferase reporter assay and expression of p53 and bcl-2 was detected by Western blot.Results　LMP1 induced p53 expression via NF-κB signaling pathway. Induction of p53 expression could be blocked by phosphorothiate analogs of antisense oligonucleotides to NF-κB p65 and LMP1, but not by NF-κB p50. However, it seemed that LMP1 had no influence on bcl-2 expression in nasopharyngeal carcinoma.ConclusionInduction expression of p53 by EBV- encoded LMP1 implies that p53 may act as a mediator in apoptosis triggered by LMP1, which brings about a complex balance in nasopharngeal carcinogenesis.