miR-26b Inhibits Virus Replication Through Positively miR-26b Inhibits Virus Replication Through Positively
miR-26b Inhibits Virus Replication Through Positively miR-26b Inhibits Virus Replication Through Positively
复制标题
miR-26b 通过积极抑制病毒复制 miR-26b 通过积极抑制病毒复制
作者：
Chang Liu;Liting Zhang;Rui Xu;Hui Zheng
据报道，microRNA 在各种生物过程中发挥着至关重要的作用，包括细胞增殖、细胞凋亡、肿瘤发生和病毒感染。已发现miR-26b参与多种肿瘤的发病机制，然而，对其在先天免疫反应中所起的作用知之甚少。在这项研究中，我们报告说 miR-26b 能够诱导 I 型干扰素 (IFN) 表达，这得到了定量实时聚合酶链反应和荧光素酶报告基因检测的支持。相反，抑制miR-26b后IFN的产生减少。随后，miR-26b 的异位表达导致 STAT1 和 IFN 刺激基因 (ISG) 的表达上调。此外，miR-26b 的过表达抑制了水泡性口炎病毒（VSV）和仙台病毒（SeV）的复制。反过来，IFN能够以时间依赖性方式诱导miR-26b的表达。总之，我们发现miR-26b可以通过上调I型IFN和ISG来抑制VSV复制，并且反过来可以被IFN上调。
microRNAs have been reported to play crucial roles in various biological processes, including cell proliferation,.apoptosis, tumor genesis, and viral infections. miR-26b has been found to be involved in the pathogenesis of.multiple tumors, however, little is known about the role it plays in innate immune responses. In this study, we.report that miR-26b is able to induce type-I interferon (IFN) expression, which was supported by both quantitative.real time polymerase chain reaction and luciferase reporter assays. Conversely, production of IFN was.reduced upon inhibition of miR-26b. Sequentially, ectopic expression of miR-26b led to upregulated expression.of STAT1 and IFN-stimulated genes (ISGs). Furthermore, overexpression of miR-26b repressed the replication.of vesicular stomatitis virus (VSV) and Sendai virus (SeV). In turn, IFN was able to induce the expression of.miR-26b in a time-dependent manner. In all, we found that miR-26b could inhibit VSV replication through.upregulation of type-I IFNs and ISGs and could in turn be upregulated by IFNs.