Liao W, Tang M, Yin L
Cancer Research Institute, Hunan Medical University, Changsha, Hunan 410078, China.
Zhonghua Zhong Liu Za Zhi. 2001 May;23(3):199-201.
To ascertain if EBV-encoded latent membrane protein 1 (LMP1) induces p53 expression via NF-kappa B signaling.
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-kappa B was determined by luciferase reporter assay and expression of p53 and bcl-2 was detected by Western blot.
LMP1 induced p53 expression via NF-kappa B signaling pathway. Induction of p53 expression could be blocked by phosphorothiate analogs of antisense oligonucleotides to NF-kappa B p65 and LMP1, but not by NF-kappa B p50. However, it seemed that LMP1 had no influence on bcl-2 expression in nasopharyngeal carcinoma.
Induction 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 nasopharyngeal carcinogenesis.
确定EB病毒编码的潜伏膜蛋白1（LMP1）是否通过核因子κB（NF-κB）信号传导诱导p53表达。
本研究使用了一种经四环素调控LMP1表达的鼻咽癌细胞系Tet-on-LMP1 HNE2，该细胞系已转染LMP1。通过荧光素酶报告基因检测法测定NF-κB的功能活性，并用蛋白质免疫印迹法检测p53和bcl-2的表达。
LMP1通过NF-κB信号通路诱导p53表达。针对NF-κB p65和LMP1的反义寡核苷酸硫代磷酸酯类似物可阻断p53表达的诱导，但NF-κB p50则不能。然而，LMP1似乎对鼻咽癌中bcl-2的表达没有影响。
EB病毒编码的LMP1诱导p53表达意味着p53可能在LMP1触发的细胞凋亡中起介导作用，这在鼻咽癌发生过程中产生了复杂的平衡。
