首页> 外文期刊>Chinese Medical Journal >Epstein-Barr virus encoded latent membrane protein 1 induces TRAF1 expression to promote anti-apoptosis activity via NF-κB signaling pathway in nasopharyngeal carcinoma
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Epstein-Barr virus encoded latent membrane protein 1 induces TRAF1 expression to promote anti-apoptosis activity via NF-κB signaling pathway in nasopharyngeal carcinoma

机译:爱泼斯坦-巴尔病毒编码的潜伏膜蛋白1通过鼻咽癌中的NF-κB信号通路诱导TRAF1表达以促进抗凋亡活性

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摘要

Objectives To identify whether Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor-associated factor 1 (TRAF1) expression and promote its anti-apoptosis activity via the NF-κB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC). Methods A stable transfected cell line HNE2-LMP1 was established by introducing LMP1 cDNA into HNE2 cells. Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT-PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis. Apoptosis activity was observed through fluorescence staining. Results LMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis. This induction could be blocked by antisense LMP1. Moreover, LMP1-mediated induction of a TRAF1 promoter-driven reporter gene was significantly impaired when the κB site κB1 or κB5 was disrupted, whereas mutation of κB3 had only a minor effect on LMP1 dependent up-regulation of the reporter gene. Conclusion LMP1 induces TRAF1 expression and promotes its anti-apoptosis activity via the NF-κB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells.
机译:目的确定爱泼斯坦巴尔病毒(EBV)编码的潜伏膜蛋白1(LMP1)是否可以诱导肿瘤坏死因子受体相关因子1(TRAF1)的表达并通过NF-κB信号通路促进其抗凋亡活性,并进行评估LMP1抑制鼻咽癌(NPC)的凋亡。方法通过将LMP1 cDNA导入HNE2细胞,建立稳定的转染细胞系HNE2-LMP1。荧光素酶报告基因检测TRAF1的反式激活,而RT-PCR检测TRAF1 mRNA的表达,蛋白质印迹法检测TRAF1蛋白和胱天蛋白酶3的表达。通过荧光染色观察细胞凋亡活性。结果LMP1诱导NPC细胞中TRAF1表达,并导致细胞凋亡减少。该诱导可以被反义LMP1阻断。此外,当κB位点κB1或κB5受到破坏时,LMP1介导的TRAF1启动子驱动的报告基因的诱导显着受损,而κB3的突变对依赖LMP1的报告基因上调的影响很小。结论LMP1通过NF-κB信号通路诱导TRAF1表达并增强其抗凋亡活性,这可能是LMP1抑制NPC细胞凋亡的机制之一。

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