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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >MicroRNAs-372/373 Promote the Expression of Hepatitis B Virus Through the Targeting of Nuclear Factor I/B
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MicroRNAs-372/373 Promote the Expression of Hepatitis B Virus Through the Targeting of Nuclear Factor I/B

机译：MicroRNAs-372 / 373通过靶向核因子I / B促进乙型肝炎病毒的表达

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摘要

MicroRNAs (miRNAs) play important roles in the posttranscriptional regulation of gene expression. Recent evidence has indicated the pathological relevance of miRNA dysregula-tion in hepatitis virus infection; however, the roles of microRNAs in the regulation of hepatitis B virus (HBV) expression are still largely unknown. In this study we identified that miR-373 was up-regulated in HBV-infected liver tissues and that the members of the miRs-371-372-373 (miRs-371-3) gene cluster were also significantly co-up-regulated in HBV-producing HepG2.2.15 cells. A positive in vivo association was identified between hepatic HBV DNA levels and the copy number variation of the miRs-371-3 gene cluster. The enhanced expression of miRs-372/373 stimulated the production of HBV proteins and HBV core-associated DNA in HepG2 cells transfected with 1.3 X HBV. Further, nuclear factor I/B (NFIB) was identified to be a direct functional target of miRs-372/373 by in silico algorithms and this was subsequently confirmed by western blotting and luciferase reporter assays. Knockdown of NFIB by small interfering RNA (siRNA) promoted HBV expression, whereas rescue of NFIB attenuated the stimulation in the 1.3 X HBV-transfected HepG2 cells. Conclusion: Our study revealed that miRNA (miRs-372/373) can promote HBV expression through a pathway involving the transcription factor (NFIB). This novel model provides new insights into the molecular basis in HBV and host interaction.
机译：MicroRNA（miRNA）在基因表达的转录后调控中发挥重要作用。最近的证据表明，miRNA失调与肝炎病毒感染的病理相关性。然而，microRNA在调节乙型肝炎病毒（HBV）表达中的作用仍然未知。在这项研究中，我们发现miR-373在HBV感染的肝组织中被上调，并且miRs-371-372-373（miRs-371-3）基因簇的成员在HBV感染的肝脏中也被显着上调。产生HBV的HepG2.2.15细胞。在肝脏HBV DNA水平和miRs-371-3基因簇的拷贝数变异之间鉴定出阳性的体内关联。 miRs-372 / 373的表达增强刺激了转染1.3 X HBV的HepG2细胞中HBV蛋白和HBV核心相关DNA的产生。此外，通过计算机模拟，已将核因子I / B（NFIB）鉴定为miRs-372 / 373的直接功能靶标，随后通过蛋白质印迹法和荧光素酶报告基因检测法证实了这一点。通过小干扰RNA（siRNA）抑制NFIB可以促进HBV表达，而拯救NFIB可以减弱1.3 X HBV转染的HepG2细胞的刺激。结论：我们的研究表明，miRNA（miRs-372 / 373）可以通过涉及转录因子（NFIB）的途径促进HBV表达。这种新颖的模型为HBV和宿主相互作用的分子基础提供了新见解。

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