Document Detail

Epstein-Barr virus-induced epigenetic alterations following transient infection.
MedLine Citation:
PMID:  23047626     Owner:  NLM     Status:  MEDLINE    
Epstein-Barr virus (EBV) is a known tumor virus associated with an increasing array of malignancies; however, the association of the virus with certain malignancies is often erratic. To determine EBV's contributions to tumorigenesis in a setting of incomplete association, a transient model of infection was established where a clonal CCL185 carcinoma cell line infected with recombinant EBV was allowed to lose viral genomes by withdrawal of selection pressure. Global gene expression comparing EBV-negative, transiently infected clones to uninfected controls identified expression changes in more than 1,000 genes. Among downregulated genes, several genes known to be deoxyribonucleic acid (DNA) methylated in cancer were identified including E-cadherin and PYCARD. A cadherin switch, increased motility and enhanced cellular invasiveness present in EBV-positive cells were retained after viral loss, indicating an epigenetic effect. Repression of PYCARD expression was a result of increased promoter CpG methylation, whereas loss of E-cadherin expression after transient EBV infection did not correlate with increased DNA methylation of the E-cadherin promoter. Rather, repression of E-cadherin was consistent with the formation of a repressive chromatin state. Decreased histone 3 or 4 acetylation at the promoter and 5' end of the E-cadherin gene was observed in an EBV-negative, transiently infected clone relative to the uninfected controls. These results suggest that EBV can stably alter gene expression in a heritable fashion in formerly infected cells, whereas its own contribution to the oncogenic process is masked.
Krista J Queen; Mingxia Shi; Fangfang Zhang; Urska Cvek; Rona S Scott
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-11-02
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  132     ISSN:  1097-0215     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-02-19     Completed Date:  2013-05-07     Revised Date:  2014-05-08    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2076-86     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 UICC.
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MeSH Terms
Blotting, Western
Cadherins / genetics,  metabolism
Cell Adhesion
Cell Movement
Cell Proliferation
Chromatin / genetics*
Chromatin Immunoprecipitation
CpG Islands
Cytoskeletal Proteins / genetics,  metabolism
DNA Methylation*
Epstein-Barr Virus Infections / genetics*,  pathology,  virology
Gene Expression Profiling
Herpesvirus 4, Human / pathogenicity*
Histones / metabolism
Lung Neoplasms / genetics*,  pathology,  virology
Oligonucleotide Array Sequence Analysis
Promoter Regions, Genetic / genetics
RNA, Messenger / genetics
Real-Time Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Tumor Markers, Biological / genetics*,  metabolism
Grant Support
Reg. No./Substance:
0/Cadherins; 0/Chromatin; 0/Cytoskeletal Proteins; 0/Histones; 0/PYCARD protein, human; 0/RNA, Messenger; 0/Tumor Markers, Biological

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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