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Epstein-Barr virus-induced epigenetic alterations following transient infection.
Int J Cancer 2013; 132(9):2076-86IJ

Abstract

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.

Authors+Show Affiliations

Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

23047626

Citation

Queen, Krista J., et al. "Epstein-Barr Virus-induced Epigenetic Alterations Following Transient Infection." International Journal of Cancer, vol. 132, no. 9, 2013, pp. 2076-86.
Queen KJ, Shi M, Zhang F, et al. Epstein-Barr virus-induced epigenetic alterations following transient infection. Int J Cancer. 2013;132(9):2076-86.
Queen, K. J., Shi, M., Zhang, F., Cvek, U., & Scott, R. S. (2013). Epstein-Barr virus-induced epigenetic alterations following transient infection. International Journal of Cancer, 132(9), pp. 2076-86. doi:10.1002/ijc.27893.
Queen KJ, et al. Epstein-Barr Virus-induced Epigenetic Alterations Following Transient Infection. Int J Cancer. 2013 May 1;132(9):2076-86. PubMed PMID: 23047626.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epstein-Barr virus-induced epigenetic alterations following transient infection. AU - Queen,Krista J, AU - Shi,Mingxia, AU - Zhang,Fangfang, AU - Cvek,Urska, AU - Scott,Rona S, Y1 - 2012/11/02/ PY - 2012/04/05/received PY - 2012/09/14/accepted PY - 2012/10/11/entrez PY - 2012/10/11/pubmed PY - 2013/5/8/medline SP - 2076 EP - 86 JF - International journal of cancer JO - Int. J. Cancer VL - 132 IS - 9 N2 - 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. SN - 1097-0215 UR - https://www.unboundmedicine.com/medline/citation/23047626/Epstein_Barr_virus_induced_epigenetic_alterations_following_transient_infection_ L2 - https://doi.org/10.1002/ijc.27893 DB - PRIME DP - Unbound Medicine ER -