Avian leukosis virus subgroup J induces VEGF expression via NF-kappa B/PI3K-dependent IL-6 production

文献类型： 外文期刊

第一作者： Gao, Yanni

作者： Gao, Yanni;Zhang, Yao;Guan, Xiaolu;Liu, Yongzhen;Qi, Xiaole;Wang, Yongqiang;Liu, Changjun;Zhang, Yanping;Gao, Honglei;Wang, Xiaomei;Gao, Yulong;Yao, Yongxiu;Nair, Venugopal;Yao, Yongxiu;Nair, Venugopal

作者机构：

关键词： ALV-J;interleukin 6;tumorigenesis;VEGF-A;VEGFR-2;Immunology and Microbiology Section;Immune response;Immunity

期刊名称：ONCOTARGET （ 影响因子：5.168； 五年影响因子：5.312 ）

ISSN： 1949-2553

年卷期： 2016 年 7 卷 49 期

页码：

收录情况： SCI

摘要： Avian leukosis virus subgroup J (ALV-J) is an oncogenic virus causing hemangiomas and myeloid tumors in chickens. Interleukin-6 (IL-6) is a multifunctional pro-inflammatory interleukin involved in many types of cancer. We previously demonstrated that IL-6 expression was induced following ALV-J infection in chickens. The aim of this study is to characterize the mechanism by which ALV-J induces IL-6 expression, and the role of IL-6 in tumor development. Our results demonstrate that ALV-J infection increases IL-6 expression in chicken splenocytes, peripheral blood lymphocytes, and vascular endothelial cells. IL-6 production is induced by the ALV-J envelope protein gp85 and capsid protein p27 via PI3K- and NF-kappa B-mediated signaling. IL-6 in turn induced expression of vascular endothelial growth factor (VEGF)-A and its receptor, VEGFR-2, in vascular endothelial cells and embryonic vascular tissues. Suppression of IL-6 using siRNA inhibited the ALV-J induced VEGF-A and VEGFR-2 expression in vascular endothelial cells, indicating that the ALV-J-induced VEGF-A/VEGFR-2 expression is mediated by IL-6. As VEGF-A and VEGFR-2 are important factors in oncogenesis, our findings suggest that ALV-J hijacks IL-6 to promote tumorigenesis, and indicate that IL-6 could potentially serve as a therapeutic target in ALV-J infections.

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