PDF(Pubmed)
Abstract：
UNASSIGNED: The 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.
UNASSIGNED: The 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.
UNASSIGNED: The 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.
UNASSIGNED: Our 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.
UNASSIGNED: The 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.
UNASSIGNED: The 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.
UNASSIGNED: Our 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.
摘要：
未经证实：肠道病毒D68（EV-D68）的流行增加了对该病毒作为能够引起严重呼吸道和神经系统疾病的病原体的认识。已经显示长链非编码RNA(lncRNA)通过多种机制或信号通路调节病毒复制和感染。然而,lncRNAs在EV-D68感染中的确切功能仍然未知.
UNASSIGNED：使用高通量测序技术研究了EV-D68感染和未感染的横纹肌肉瘤（RD）细胞中lncRNA的差异表达谱。通过小干扰RNA（siRNA）的敲低和lncRNASNHG9（小核糖核酸宿主基因9）的过表达用于研究lncRNASNHG9如何调节EV-D68繁殖。使用双荧光素酶报告系统验证了lncRNASNHG9与miR-150-5p和miR-150-5p与c-Fos的靶向相互作用。将LncRNASNHG9敲低和miR-150-5p抑制剂与RD细胞共转染。QRT-PCR和Westernblot检测RNA和蛋白质水平,分别为c-Fos和VP1。应用中位组织培养感染剂量(TCID50)来检测病毒滴度。
UNASSIGNED：结果表明，在EV-D68感染模型中，总共375个lncRNA高度失调。在EV-D68感染模型中,在EV-D68感染的RD细胞中，lncRNASNHG9和c-Fos增加。然而,miR-150-5p的表达水平下调。此外,在RD细胞中SNHG9的过表达导致EV-D68感染后病毒复制水平和病毒滴度降低,进一步的实验显示SNHG9的过表达通过靶向增加的miR-150-5p结合和显著增加RD细胞中的c-Fos表达来抑制病毒复制.
UNASSIGNED：我们的发现表明SNHG9/miR-150-5p/c-Fos轴影响宿主细胞中EV-D68的复制，并且SNHG9可能是抗EV-D68感染治疗的可能靶标。
UNASSIGNED：使用高通量测序技术研究了EV-D68感染和未感染的横纹肌肉瘤（RD）细胞中lncRNA的差异表达谱。通过小干扰RNA（siRNA）的敲低和lncRNASNHG9（小核糖核酸宿主基因9）的过表达用于研究lncRNASNHG9如何调节EV-D68繁殖。使用双荧光素酶报告系统验证了lncRNASNHG9与miR-150-5p和miR-150-5p与c-Fos的靶向相互作用。将LncRNASNHG9敲低和miR-150-5p抑制剂与RD细胞共转染。QRT-PCR和Westernblot检测RNA和蛋白质水平,分别为c-Fos和VP1。应用中位组织培养感染剂量(TCID50)来检测病毒滴度。
UNASSIGNED：结果表明，在EV-D68感染模型中，总共375个lncRNA高度失调。在EV-D68感染模型中,在EV-D68感染的RD细胞中，lncRNASNHG9和c-Fos增加。然而,miR-150-5p的表达水平下调。此外,在RD细胞中SNHG9的过表达导致EV-D68感染后病毒复制水平和病毒滴度降低,进一步的实验显示SNHG9的过表达通过靶向增加的miR-150-5p结合和显著增加RD细胞中的c-Fos表达来抑制病毒复制.
UNASSIGNED：我们的发现表明SNHG9/miR-150-5p/c-Fos轴影响宿主细胞中EV-D68的复制，并且SNHG9可能是抗EV-D68感染治疗的可能靶标。
