Long non-coding RNA SNHG9 regulates viral replication in rhabdomyosarcoma cells infected with enterovirus D68 via miR-150-5p/c-Fos axis
作者全名："Fu, Huichao; Si, Junzhuo; Xu, Lei; Tang, Xia; He, Yonglin; Lu, Nan; Li, Huayi; Li, Anlong; Gao, Sijia; Yang, Chun"
作者地址："[Fu, Huichao; Si, Junzhuo; Xu, Lei; He, Yonglin; Lu, Nan; Li, Huayi; Li, Anlong; Gao, Sijia; Yang, Chun] Chongqing Med Univ, Coll Basic Med, Dept Pathogen Biol, Chongqing, Peoples R China; [Tang, Xia] Rongchang Dist Peoples Hosp, Chongqing, Peoples R China"
通信作者："Yang, C (通讯作者)，Chongqing Med Univ, Coll Basic Med, Dept Pathogen Biol, Chongqing, Peoples R China."
来源：FRONTIERS IN MICROBIOLOGY
关键词：enterovirus D68; SNHG9; miR-150-5p; c-Fos; infection; ceRNA
摘要："BackgroundThe Enterovirus D68 (EV-D68) epidemic has increased knowledge of the virus as a pathogen capable of causing serious respiratory and neurological illnesses. It has been shown that long noncoding RNAs (lncRNAs) regulate viral replication and infection via multiple mechanisms or signaling pathways. However, the precise function of lncRNAs in EV-D68 infection remains unknown. MethodsThe differential expression profiles of lncRNA in EV-D68-infected and uninfected rhabdomyosarcoma (RD) cells were studied using high-throughput sequencing technology. The knockdown through small interfering RNA (siRNA) and overexpression of lncRNA SNHG9 (small ribonucleic acid host gene 9) were applied to investigate how lncRNA SNHG9 regulates EV-D68 propagation. The targeted interactions of lncRNA SNHG9 with miR-150-5p and miR-150-5p with c-Fos were validated using dual luciferase reporter system. LncRNA SNHG9 knockdown and miR-150-5p inhibitor were co-transfected with RD cells. QRT-PCR and western blot were used to detect RNA and protein levels, of c-Fos and VP1, respectively. Median tissue culture infectious dose (TCID50) was applied to detect viral titers. ResultsThe results demonstrated that a total of 375 lncRNAs were highly dysregulated in the EV-D68 infection model. In the EV-D68 infection model, lncRNA SNHG9 and c-Fos were increased in EV-D68-infected RD cells. However, the expression level of miR-150-5p was downregulated. In addition, overexpression of SNHG9 in RD cells resulted in decreased viral replication levels and viral titers following infection with EV-D68, and further experiments revealed that overexpression of SNHG9 inhibited the viral replication by targeting increased miR-150-5p binding and significantly increased c-Fos expression in RD cells. ConclusionOur findings indicate that the SNHG9/miR-150-5p/c-Fos axis influences EV-D68 replication in host cells and that SNHG9 may be a possible target for anti-EV-D68 infection therapies."
基金机构：Natural Science Foundation of Chongqing [cstc2017jcyjAX0409]; Graduate Training Fund of Chongqing Medical University
基金资助正文："Funding This work was funded by Natural Science Foundation of Chongqing (cstc2016jcyjA0212), Natural Science Foundation of Chongqing (cstc2017jcyjAX0409), and Graduate Training Fund of Chongqing Medical University."