Marek's disease virus-encoded analog of microRNA-155 activates the oncogene c-Myc by targeting LTBP1 and suppressing the TGF-beta signaling pathway

文献类型: 外文期刊

第一作者: Chi, Jia-Qi

作者: Chi, Jia-Qi;Yu, Zu-Hua;Chi, Jia-Qi;Teng, Man;Yu, Zu-Hua;Su, Jing-Wei;Zhao, Pu;Xing, Guang-Xu;Deng, Rui-Guang;Luo, Jun;Su, Jing-Wei;Zhao, Pu;Liang, Hong-De;Zhang, Gai-Ping;Qu, Liang-Hu;Zhang, Gai-Ping

作者机构:

关键词: MicroRNA;MDV;miR-155;mdv1-miR-M4-5p;LTBP1;TGF-beta signaling;Oncogenesis

期刊名称:VIROLOGY ( 影响因子:3.616; 五年影响因子:3.967 )

ISSN:

年卷期:

页码:

收录情况: SCI

摘要: Marek's disease virus (MDV) is a representative alpha herpes virus able to induce rapid-onset T-cell lymphoma in its natural host and regarded as an ideal model for the study of virus-induced tumorigenesis. Recent studies have shown that the mdv1-miR-M4-5p, a viral analog of cellular miR-155, is critical for MDV's oncogenicity. However, the precise mechanism whereby it was involved in MD lymphomagenesis remained unknown. We have presently identified the host mRNA targets of mdv1-miR-M4-5 and identified the latent TGF-beta binding protein 1 (LTBP1) as a critical target for it. We found that during MDV infection, down-regulation of LTBP1 expression by mdv1-miR-M4-5p led to a significant decrease of the secretion and activation of TGF-beta 1, with suppression of TGF-beta signaling and a significant activation of expression of c-Myc, a well-known oncogene which is critical for virus-induced tumorigenesis. Our findings reveal a novel and important mechanism of how mdv1-miR-M4-5p potentially contributes to MDV-induced tumorigenesis. (C) 2014 The Authors. Published by Elsevier Inc.

分类号: R37

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