alexa Up-Regulation of Lamin A/C Expression in Epstein-Barr V
ISSN: 1948-5948

Journal of Microbial & Biochemical Technology
Open Access

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Research Article

Up-Regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype

Ferenc Banati1, Anita Koroknai2, Kalman Szenthe1, Tamas Tereh2, Anita Hidasi2, Barbara Bankuti1, Krisztina Buzas3, Frederic Lemnitzer4, Zsolt Ruzsics5, Susan Szathmary6, Hans Wolf7, Daniel Salamon8, Janos Minarovits3* and Hans-Helmut Niller7

1RT-Europe Nonprofit Research Ltd., Mosonmagyaróvár, Hungary

2Microbiological Research Group, National Center for Epidemiology, Hungary

3Department of Oral Biology and Experimental Dental Research, University of Szeged, Hungary

4Max von Pettenkofer-Institut, Ludwig-Maximilians-Universität München, Germany

5University of Freiburg, University Medical Center Freiburg, Institute of Virology, Germany

6Galen-Bio Kft., Bartók Béla út 51. I/4, Budapest, H-1114, Hungary

7University of Regensburg, Franz-Josef-Strauss Allee 11, Regensburg, D-93053, Germany

8Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden

*Corresponding Author:
Janos M
Department of Oral Biology and Experimental Dental Research
University of Szeged, Hungary
Tel: 36703948279
E-mail: [email protected]

Received date: April 27, 2017; Accepted date: May 15, 2017; Published date: May 22, 2017

Citation: Banati F, Koroknai A, Szenthe K, Tereh T, Hidasi A, et al. (2017) Up-Regulation of Lamin A/C Expression in Epstein-BarrVirus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype. J Microb Biochem Technol 9:087-094. doi:10.4172/1948-5948.1000349

Copyright: © 2017 Banati F, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Lamin A, B and C, the nuclear intermediate-filament proteins, play a role in epigenetic regulation. Lamin B could be detected in all nucleated cells studied, whereas the lamin A and lamin C isoforms (lamin A/C) encoded by the LMNA gene are co-expressed in most somatic cell types except mature B lymphocytes. Since Epstein-Barr virus (EBV), a human gammaherpesvirus, is associated with tumorigenic processes and is known to alter the epigenotype of its host cells, we studied the expression of the LMNA gene and its epigenetic marks in EBV-carrying human lymphoid cell lines. We observed a high lamin A/C mRNA expression in EBV-immortalized B lymphoblastoid cell lines (LCLs) and in a subset of Burkitt lymphoma (BL) lines characterized by an activated B cell phenotype and a unique latent EBV gene expression pattern (latency III). In these cells the first exon of LMNA was hypomethylated and associated with activating histone marks. In contrast, we observed a low level of lamin A/C mRNA expression in EBV negative BL lines and BL lines with a restricted expression of latent EBV products (latency I). Low LMNA promoter activity was associated with hypermethylation of the LMNA first exon. These data suggest a role for EBV latency products in switching on or upregulating the LMNA promoter (LMNAp) in EBV-infected activated B cells in vitro. Lamin A/C may contribute to the establishment of the activated B cell phenotype. Our data also imply a role of LMNA first exon methylation in the silencing of LMNAp.

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