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Epigenetic silencing of tumor suppressor genes during in vitro Epstein-Barr virus infection

Abhik Saha1, Hem C Jha1, Santosh K Upadhyay1

  • 1Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.

Proceedings of the National Academy of Sciences of the United States of America
|September 2, 2015
PubMed

Insights

Epstein-Barr virus (EBV) infection causes DNA hypermethylation, silencing tumor suppressor genes (TSGs) in B lymphocytes. This epigenetic change offers potential prognostic markers and therapeutic targets for EBV-associated cancers.

Area of Science:

  • Epigenetics and Molecular Biology
  • Virology
  • Cancer Research

Background:

  • DNA methylation at CpG islands is a key epigenetic regulator of gene expression in mammals.
  • Aberrant methylation, including oncogene activation and tumor suppressor gene (TSG) silencing, drives human cancer development.
  • Epigenetic modifications influence viral genomes and host cells in virus-associated cancers, such as Epstein-Barr virus (EBV).

Purpose of the Study:

  • To investigate the impact of EBV infection on TSG expression and epigenetic modifications in B lymphocytes.
  • To examine methylation patterns in the regulatory sequences of TSGs following EBV infection.
  • To explore the potential of TSG methylation profiles as biomarkers and therapeutic targets for EBV-related diseases.

Main Methods:

  • Infection of primary human B lymphocytes with EBV.
  • Analysis of TSG expression patterns.
  • Assessment of epigenetic modifications, specifically CpG methylation in TSG regulatory regions.

Main Results:

  • EBV infection induced global transcriptional repression of a comprehensive panel of TSGs.
  • This repression was mediated by increased DNA hypermethylation in the regulatory sequences of TSGs.
  • Proliferation of EBV-infected B lymphocytes (lymphoblastoid cell lines) correlated with these epigenetic changes.

Conclusions:

  • EBV infection triggers widespread TSG silencing via DNA hypermethylation in B lymphocytes.
  • CpG methylation profiles of TSGs represent promising prognostic markers for EBV-associated conditions.
  • Targeting these methylation patterns could lead to novel therapeutic strategies for EBV infections and lymphomas.
Keywords:
B-cell lymphomaEBVlymphoblastoid cell linespromoter methylationtumor suppressor genes

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