Avian leukosis virus subgroup J promotes cell proliferation and cell cycle progression through miR-221 by targeting CDKN1B

文献类型： 外文期刊

第一作者： Ren, Chaoqi

作者： Ren, Chaoqi;Yu, Mengmeng;Zhang, Yao;Fan, Minghui;Chang, Fangfang;Xing, Lixiao;Liu, Yongzhen;Wang, Yongqiang;Qi, Xiaole;Liu, Changjun;Zhang, Yanping;Cui, Hongyu;Li, Kai;Gao, Li;Pan, Qing;Wang, Xiaomei;Gao, Yulong;Wang, Xiaomei

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关键词： Avian leukosis virus subgroup J; MiR-221; CDKN1B; Cell cycle

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

ISSN： 0042-6822

年卷期： 2018 年 519 卷

页码：

收录情况： SCI

摘要： Avian leukosis virus subgroup J (ALV-J), a highly oncogenic retrovirus, causes leukemia-like proliferative diseases in chickens. microRNAs post-transcriptionally suppress targets and are involved in the development of various tumors. We previously showed that miR-221 is upregulated in ALV-J-induced tumors. In this study, we analyzed the possible function of miR-221 in ALV-J tumorigenesis. The target validation system showed that CDKN1B is a target of miR-221 and is downregulated in ALV-J infection. As CDKN1B arrests the cell cycle and regulates its progression, we analyzed the proliferation of ALV-J-infected DF-1 cells. ALV-J-infection-induced DF1 cell derepression of G1/S transition and overproliferation required high miR-221 expression followed by CDKN1B downregulation. Cell cycle pathway analysis showed that ALV-J infection induced DF-1 cell overproliferation via the CDKN1B-CDK2/CDK6 pathway. Thus, miR-221 may play an important role in ALV-J-induced aggressive growth of DF-1 cells; these findings have expanded our insights into the mechanism underlying ALV-J infection and tumorigenesis.

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