Over-expression of human cytomegalovirus miR-US25-2-3p downregulates eIF4A1 and inhibits HCMV replication

Over-expression of human cytomegalovirus miR-US25-2-3p downregulates eIF4A1 and inhibits HCMV replication
复制标题

人巨细胞病毒 miR-US25-2-3p 的过表达下调 eIF4A1 并抑制 HCMV 复制

DOI:
10.1016/j.febslet.2013.05.057
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发表时间:
2013-07-11
期刊:
影响因子:
3.5
通讯作者:
Ruan, Qiang
Ruan, Qiang
中科院分区:
生物学3区
文献类型:
--
作者:
Qi, Manlong;Qi, Ying;Ruan, Qiang

文献摘要

被引文献

相似文献

已有研究表明,人巨细胞病毒(HCMV)miR-US25-2可抑制包括HCMV在内的DNA病毒复制。然而,其机制仍不清楚。在我们的研究中,真核细胞翻译起始因子4A1(EIF4A1)被确定为miR-US25-2-3p的直接靶标。小干扰RNA(SiRNA)和miR-US25-2-3p介导的eIF4A1基因敲除实验表明,MRC-5细胞中高水平的miR-US25-2-3p抑制了HCMV和宿主基因组DNA的合成,并抑制了帽依赖的翻译和宿主细胞的增殖。然而,miR-US25-2-3p抑制剂诱导的eIF4A1上调使HCMV拷贝数增加。因此,miR-US25-2-3p的过度表达和eIF4A1的低表达可能有助于抑制HCMV的复制。(C)2013年欧洲生化学会联合会。爱思唯尔出版,版权所有。
It has been reported that human cytomegalovirus (HCMV) miR-US25-2 reduces DNA viral replication including HCMV. However, the mechanism remains unknown. In our study, eukaryotic translation initiation factor 4A1 (eIF4A1) was identified to be a direct target of miR-US25-2-3p. Small interfering RNA (siRNA) and miR-US25-2-3p mediated eIF4A1 knockdown experiments revealed that high level of miR-US25-2-3p in MRC-5 cells decreased HCMV and host genomic DNA synthesis, and inhibited cap-dependent translation and host cell proliferation. However, eIF4A1 up-regulation induced by miR-US25-2-3p inhibitor increased HCMV copy number. Therefore, the over-expression of miR-US25-2-3p and consequent lower expression of eIF4A1 may contribute to the inhibition of HCMV replication. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.