Virus-encoded miR-155 ortholog in Marek's disease virus promotes cell proliferation via suppressing apoptosis by targeting tumor suppressor WWOX

文献类型： 外文期刊

第一作者： Zhu, Zhi-Jian

作者： Zhu, Zhi-Jian;Teng, Man;Li, Hui-Zhen;Zheng, Lu-Ping;Liu, Jin-Ling;Luo, Jun;Zhu, Zhi-Jian;Teng, Man;Li, Hui-Zhen;Zheng, Lu-Ping;Liu, Jin-Ling;Luo, Jun;Zhu, Zhi-Jian;Teng, Man;Li, Hui-Zhen;Zheng, Lu-Ping;Liu, Jin-Ling;Luo, Jun;Zhu, Zhi-Jian;Li, Hui-Zhen;Zhang, Gai-Ping;Yao, Yongxiu;Nair, Venugopal;Yao, Yongxiu;Nair, Venugopal;Zhang, Gai-Ping;Luo, Jun

作者机构：

关键词： Herpesvirus; MDV-1; Oncogenesis; microRNA-155; miR-M4-5p; WWOX; Apoptosis

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

ISSN： 0378-1135

年卷期： 2021 年 252 卷

页码：

收录情况： SCI

摘要： Marek's disease virus serotype 1 (MDV-1) is an important oncogenic a-herpesvirus that induces immunosuppressive and rapid-onset T-cell lymphomatous disease in poultry commonly referred to as Marek's disease (MD). As an excellent biomodel for the study of virally-induced cancers in natural hosts, MDV-1 encoded microRNAs (miRNAs) have been previously demonstrated with the potential roles to act as critical regulators in virus replication, latency, pathogenesis and especially in oncogenesis. Similar to the oncogenic y-herpesvirus Kaposi's sarcoma-associated herpesvirus (KSHV), miR-M4-5p, the cellular microRNA-155 (miR-155) ortholog encoded by MDV-1, is also involved in MD oncogenesis. In lymphoblastoid cell lines derived from MDV-induced T-cell lymphomas, miR-M4-5p has been shown to be highly expressed and participate in inducing MD lymphomagenesis by regulating multiple signal pathways. Herein we report the new identification of the host WW domain-containing oxidoreductase (WWOX) as a biological target for miR-M4-5p. Further experiments revealed that as a critical oncomiRNA, miR-M4-5p promotes the proliferations of both chicken embryo fibroblast (CEF) and MSB-1 cells via suppressing cell apoptosis by targeting WWOX, a well-known tumor suppressor. Our data presents a novel insight in elucidating the regulatory mechanisms mediated by the viral analog of miR-155 that potentially contribute to MD tumorigenesis.

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