STAT3 activation induced by Epstein-Barr virus latent membrane protein1 causes vascular endothelial growth factor expression and cellular invasiveness via JAK3 And ERK signaling
STAT3 activation induced by Epstein-Barr virus latent membrane protein1 causes vascular endothelial growth factor expression and cellular invasiveness via JAK3 And ERK signaling
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Epstein-Barr病毒潜伏膜蛋白1诱导的STAT3激活通过JAK3和ERK信号传导导致血管内皮生长因子表达和细胞侵袭
DOI：
10.1016/j.ejca.2010.07.008
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发表时间：
2010-11-01
影响因子：
8.4
通讯作者：
Cao, Ya
中科院分区：
文献类型：
--
作者：
Wang, Zhenlian;Luo, Feijun;Cao, Ya
主要的 Epstein-Barr 病毒 (EBV) 癌蛋白潜膜蛋白 1 (LMP1) 被认为与鼻咽癌 (NPC) 的高度侵袭性有关。信号转导子和转录激活子 3 (STAT3) 是增殖和细胞凋亡的主要转录调节因子，并且新近与血管生成和侵袭性有关，而血管生成和侵袭性可能反过来又与血管生成和侵袭性相关。 导致鼻咽癌的高度侵袭性特征 LMP1 调节 STAT3 激活在鼻咽癌细胞侵袭中的基本分子机制尚未完全探索在此我们表明，LMP1 在 STAT3 激活后向 Janus 激酶 3 (JAK3) 和细胞外信号调节激酶 1/2 (ERK1/2) 通路发出信号以及 LMP1 诱导的 STAT 反式激活活性 血管内皮生长因子 (VEGF) 通过 JAK/STAT 和丝裂原激活蛋白激酶 (MAPK)/ERK 信号通路表达 人病毒癌蛋白 LMP1 诱导 STAT3 可能有助于鼻咽癌 (C) 2010 Elsevier Ltd 保留所有权利
The principal Epstein-Barr virus (EBV) oncoprotein latent membrane protein 1 (LMP1) has been suggested to contribute to the highly invasive nature of nasopharyngeal carcinoma (NPC) Signal transducer and activator of transcription 3 (STAT3) is a master transcriptional regulator in proliferation and apoptosis and is newly implicated in angiogenesis and invasiveness which in turn are likely to contribute to the highly invasive character of NPC The fundamental molecular mechanisms of LMP1 regulated STAT3 activation in NPC cell invasion have not been completely explored Here we showed that LMP1 signals the Janus kinase 3 (JAK3) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways upon the activation of STAT3 as well as STAT transactivation activity LMP1 induces vascular endothelial growth factor (VEGF) expression via the JAK/STAT and mitogen activated protein kinase (MAPK)/ERK signalling pathways Induction of STAT3 by the human viral oncoprotein LMP1 may contribute to the invasion of NPC (C) 2010 Elsevier Ltd All rights reserved