甲基化状态和活化蛋白1元件参与EB病毒阳性淋巴瘤细胞中EB病毒介导的miR-155表达。
Methylation status and AP1 elements are involved in EBV-mediated miR-155 expression in EBV positive lymphoma cells.
作者信息
Yin Qinyan, Wang Xia, Roberts Claire, Flemington Erik K, Lasky Joseph A
机构信息
Section of Pulmonary Diseases, Critical Care and Environmental Medicine, Department of Medicine, SL9, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
Department of Pathology and Laboratory Medicine, SL79, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
出版信息
Virology. 2016 Jul;494:158-67. doi: 10.1016/j.virol.2016.04.005. Epub 2016 Apr 26.
The relationship between Epstein Barr Virus (EBV) and miR-155 is well established. EBV infection induces miR-155 expression, which is expressed at higher levels in EBV latency type III cells compared to EBV latency type I cells. However, the mechanism by which EBV latency genes activate miR-155 expression is still unclear. Here we present data showing that DNA methylation regulates miR-155 expression. We also provide evidence that the AP1 signaling pathway is involved in EBV-mediated miR-155 activation, and that Bay11 influences signaling of the miR-155 promoter AP1 element. Lastly, we show that LMP2A, LMP1 and EBNAs cannot activate miR-155 expression alone, indicating that the regulation of miR-155 by EBV is dependent on more than one EBV gene or cell signaling pathway. We conclude that the regulation of miR-155 in EBV-positive cells occurs through multiple cell signaling processes involving EBV-mediated chromatin remodeling, cell signaling regulation and transcription factor activation.
爱泼斯坦-巴尔病毒（EBV）与miR-155之间的关系已得到充分证实。EBV感染会诱导miR-155表达，与EBV潜伏I型细胞相比，miR-155在EBV潜伏III型细胞中表达水平更高。然而，EBV潜伏基因激活miR-155表达的机制仍不清楚。在此，我们展示的数据表明DNA甲基化调节miR-155表达。我们还提供证据表明AP1信号通路参与EBV介导的miR-155激活，并且Bay11影响miR-155启动子AP1元件的信号传导。最后，我们表明LMP2A、LMP1和EBNAs不能单独激活miR-155表达，这表明EBV对miR-155的调节依赖于不止一个EBV基因或细胞信号通路。我们得出结论，EBV阳性细胞中miR-155的调节是通过多个细胞信号转导过程发生的，这些过程涉及EBV介导的染色质重塑、细胞信号调节和转录因子激活。
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