Abstract
Epigenetic modifications leading to either transcriptional repression or activation, play an indispensable role in the development of human cancers. Epidemiological study revealed that approximately 20% of all human cancers are associated with tumor viruses. Epstein-Barr virus (EBV), the first human tumor virus, demonstrates frequent epigenetic alterations on both viral and host genomes in associated cancers—both of epithelial and lymphoid origin. The cell type-dependent different EBV latent gene expression patterns appear to be determined by the cellular epigenetic machinery and similarly viral oncoproteins recruit epigenetic regulators in order to deregulate the cellular gene expression profile resulting in several human cancers. This review elucidates the epigenetic consequences of EBV–host interactions during development of multiple EBV-induced B-cell lymphomas, which may lead to the discovery of novel therapeutic interventions against EBV-associated B-cell lymphomas by alteration of reversible patho-epigenetic markings.
Highlights
Epigenetics is defined as somatically-heritable changes causing alteration in gene expression patterns that are not exclusively reliant on simple gene sequence.These alterations triggered by different external stimuli—ranging from multiple genotoxic stresses to infections caused by several intracellular pathogens, including tumor viruses—are stable and cell type-specific but may not always be heritable
The histone deacetylase (HDAC)—a subset of 11 transcripts—were, in general, markedly up-regulated by two days post-infection and maintained the level throughout the course of infection [82]. These results provide additional clues that chromatin modifying and remodeling factors may function in collaboration with methylation activities to regulate tumor suppressor genes (TSGs) expression during Epstein-Barr virus (EBV) infection of resting B-lymphocytes (RBLs)
lymphoblastoid cell lines (LCLs) provide a suitable in vitro model for exploring EBV-induced B-cell lymphomagenesis seen in those originated from immunocompromised patients suffering from post-transplant lymphoproliferative disorders (PTLDs) or several acquired immune deficiency syndrome (AIDS)-associated lymphomas [11,49,50,57]
Summary
Epigenetics is defined as somatically-heritable changes causing alteration in gene expression patterns that are not exclusively reliant on simple gene sequence (recently reviewed in [1]) These alterations triggered by different external stimuli—ranging from multiple genotoxic stresses to infections caused by several intracellular pathogens, including tumor viruses—are stable and cell type-specific but may not always be heritable. Different types of cancer engage diverse epigenetic mechanisms, ranging from an altered methylation profile at the CpG island, to histone modifications, to deregulation of DNA binding proteins in order to attenuate transcription of tumor suppressor genes while activating oncogenes [5]. Similar to the other human cancers, epigenetic modifications were shown to play a critical role in EBV-associated B-cell lymphoma development [12,13]. AIDS: acquired immune deficiency syndrome; EBV: Epstein–Barr virus; EBER: EBV-encoded small RNA; EBNA-1: Epstein–Barr nuclear antigen-1; LMP: latent membrane protein; miRNA: microRNA; Qp: BamHI Q promoter; Cp: BamHI C promoter; Wp: BamHI W promoter
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