The role of promoter methylation in Epstein-Barr virus (EBV) microRNA expression in EBV-infected B cell lines.
10.3858/emm.2011.43.7.044
- Author:
Do Nyun KIM
1
;
Yoon Jae SONG
;
Suk Kyeong LEE
Author Information
1. Research Institute of Immunobiology, Department of Medical Lifescience, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea. sukklee@catholic.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
decitabine;
DNA methylation;
Herpesvirus 4, human;
microRNAs;
promoter regions, genetic
- MeSH:
Azacitidine/analogs & derivatives/pharmacology;
B-Lymphocytes/metabolism/virology;
Cell Line;
*DNA Methylation;
DNA Modification Methylases/antagonists & inhibitors;
Gene Expression Regulation, Viral;
Gene Silencing;
Herpesvirus 4, Human/*genetics/physiology;
Humans;
MicroRNAs/genetics/*metabolism;
*Promoter Regions, Genetic;
RNA, Viral/genetics/*metabolism;
Viral Proteins/genetics
- From:Experimental & Molecular Medicine
2011;43(7):401-410
- CountryRepublic of Korea
- Language:English
-
Abstract:
Epstein-Barr virus (EBV) microRNAs (miRNAs) are expressed in EBV-associated tumors and cell lines, but the regulation mechanism of their expression is unclear yet. We investigated whether the expression of EBV miRNAs is epigenetically regulated in EBV-infected B cell lines. The expression of BART miRNAs was inversely related with the methylation level of the BART promoter at both steady-state and following 5-aza-2'-deoxycytidine treatment of the cells. The expression of BHRF1 miRNAs also became detectable with the demethylation of Cp/Wp in latency I EBV-infected cell lines. Furthermore, in vitro methylation of the BART and Cp promoters reduced the promoter-driven transactivation. In contrast, tricostatin A had little effect on the expression of EBV miRNA expression as well as on the BART and Cp/Wp promoters. Our results suggest that promoter methylation, but not histone acetylation, plays a role in regulation of the EBV miRNA expression in EBV-infected B cell lines.
