| Autor: |
Liu C; 1 Institutes of Biology and Medical Sciences, Soochow University, Soochow, Jiangsu Province, China.; 2 Department of Biology, South University of Sciences and Technology, Shenzhen, Guangdong Province, China., Zhang L; 1 Institutes of Biology and Medical Sciences, Soochow University, Soochow, Jiangsu Province, China., Xu R; 1 Institutes of Biology and Medical Sciences, Soochow University, Soochow, Jiangsu Province, China., Zheng H; 1 Institutes of Biology and Medical Sciences, Soochow University, Soochow, Jiangsu Province, China. |
| Abstrakt: |
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. |
