1. Methylation status and AP1 elements are involved in EBV-mediated miR-155 expression in EBV positive lymphoma cells.
- Author
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Yin Q, Wang X, Roberts C, Flemington EK, and Lasky JA
- Subjects
- Base Sequence, Binding Sites, Cell Line, CpG Islands, Epstein-Barr Virus Infections virology, Epstein-Barr Virus Nuclear Antigens genetics, Epstein-Barr Virus Nuclear Antigens metabolism, Gene Expression Regulation, Humans, Models, Biological, Promoter Regions, Genetic, Protein Binding, Signal Transduction, Transcription Factor AP-1 metabolism, DNA Methylation, Epstein-Barr Virus Infections genetics, Epstein-Barr Virus Infections mortality, Herpesvirus 4, Human physiology, Lymphoma etiology, MicroRNAs genetics, Response Elements
- Abstract
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., (Copyright © 2016 Elsevier Inc. All rights reserved.)
- Published
- 2016
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