Long noncoding RNA #32 contributes to antiviral responses by controlling interferon-stimulated gene expression
Long noncoding RNA #32 contributes to antiviral responses by controlling interferon-stimulated gene expression
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DOI：
10.1073/pnas.1525022113
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发表时间：
2016-09-13
影响因子：
11.1
通讯作者：
Shimotohno, Kunitada
中科院分区：
文献类型：
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作者：
Nishitsuji, Hironori;Ujino, Saneyuki;Shimotohno, Kunitada
尽管人们对长链非编码rna （lncRNAs）在生物现象中的功能有广泛的了解，但对其在宿主抗病毒反应中的作用知之甚少。在这里，我们报道IncRNA#32与I型IFN信号相关。lncRNA#32的沉默显著降低了ifn刺激基因（ISG）的表达水平，导致对脑心肌炎病毒（EMCV）感染的敏感性。相反，lncRNA#32的异位表达显著抑制EMCV复制，表明lncRNA#32正调控宿主抗病毒反应。我们进一步证实了lncRNA#32在乙型肝炎病毒和丙型肝炎病毒感染中的抑制作用。lncRNA#32结合活化转录因子2 （ATF2）并调节ISG的表达。我们的研究结果揭示了lncRNA#32在宿主抗病毒反应中的作用。
Despite the breadth of knowledge that exists regarding the function of long noncoding RNAs (lncRNAs) in biological phenomena, the role of IncRNAs in host antiviral responses is poorly understood. Here, we report that IncRNA#32 is associated with type I IFN signaling. The silencing of lncRNA#32 dramatically reduced the level of IFN-stimulated gene (ISG) expression, resulting in sensitivity to encephalomyocarditis virus (EMCV) infection. In contrast, the ectopic expression of lncRNA#32 significantly suppressed EMCV replication, suggesting that lncRNA#32 positively regulates the host antiviral response. We further demonstrated the suppressive function of lncRNA#32 in hepatitis B virus and hepatitis C virus infection. lncRNA#32 bound to activating transcription factor 2 (ATF2) and regulated ISG expression. Our results reveal a role for lncRNA#32 in host antiviral responses.