Tags

Type your tag names separated by a space and hit enter

Epigenetic silencing of tumor suppressor genes during in vitro Epstein-Barr virus infection.
Proc Natl Acad Sci U S A. 2015 Sep 15; 112(37):E5199-207.PN

Abstract

DNA-methylation at CpG islands is one of the prevalent epigenetic alterations regulating gene-expression patterns in mammalian cells. Hypo- or hypermethylation-mediated oncogene activation, or tumor suppressor gene (TSG) silencing mechanisms, widely contribute to the development of multiple human cancers. Furthermore, oncogenic viruses, including Epstein-Barr virus (EBV)-associated human cancers, were also shown to be influenced by epigenetic modifications on the viral and cellular genomes in the infected cells. We investigated EBV infection of resting B lymphocytes, which leads to continuously proliferating lymphoblastoid cell lines through examination of the expression pattern of a comprehensive panel of TSGs and the epigenetic modifications, particularly methylation of their regulatory sequences. EBV infection of primary B lymphocytes resulted in global transcriptional repression of TSGs through engagement of hypermethylation. Therefore, CpG methylation profiles of TSGs may be used as a prognostic marker as well as development of potential therapeutic strategies for controlling acute infection and EBV-associated B-cell lymphomas.

Authors+Show Affiliations

Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104 erle@upenn.edu.

Pub Type(s)

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

Language

eng

PubMed ID

26324942

Citation

Saha, Abhik, et al. "Epigenetic Silencing of Tumor Suppressor Genes During in Vitro Epstein-Barr Virus Infection." Proceedings of the National Academy of Sciences of the United States of America, vol. 112, no. 37, 2015, pp. E5199-207.
Saha A, Jha HC, Upadhyay SK, et al. Epigenetic silencing of tumor suppressor genes during in vitro Epstein-Barr virus infection. Proc Natl Acad Sci USA. 2015;112(37):E5199-207.
Saha, A., Jha, H. C., Upadhyay, S. K., & Robertson, E. S. (2015). Epigenetic silencing of tumor suppressor genes during in vitro Epstein-Barr virus infection. Proceedings of the National Academy of Sciences of the United States of America, 112(37), E5199-207. https://doi.org/10.1073/pnas.1503806112
Saha A, et al. Epigenetic Silencing of Tumor Suppressor Genes During in Vitro Epstein-Barr Virus Infection. Proc Natl Acad Sci USA. 2015 Sep 15;112(37):E5199-207. PubMed PMID: 26324942.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epigenetic silencing of tumor suppressor genes during in vitro Epstein-Barr virus infection. AU - Saha,Abhik, AU - Jha,Hem C, AU - Upadhyay,Santosh K, AU - Robertson,Erle S, Y1 - 2015/08/31/ PY - 2015/9/2/entrez PY - 2015/9/2/pubmed PY - 2016/1/5/medline KW - B-cell lymphoma KW - EBV KW - lymphoblastoid cell lines KW - promoter methylation KW - tumor suppressor genes SP - E5199 EP - 207 JF - Proceedings of the National Academy of Sciences of the United States of America JO - Proc. Natl. Acad. Sci. U.S.A. VL - 112 IS - 37 N2 - DNA-methylation at CpG islands is one of the prevalent epigenetic alterations regulating gene-expression patterns in mammalian cells. Hypo- or hypermethylation-mediated oncogene activation, or tumor suppressor gene (TSG) silencing mechanisms, widely contribute to the development of multiple human cancers. Furthermore, oncogenic viruses, including Epstein-Barr virus (EBV)-associated human cancers, were also shown to be influenced by epigenetic modifications on the viral and cellular genomes in the infected cells. We investigated EBV infection of resting B lymphocytes, which leads to continuously proliferating lymphoblastoid cell lines through examination of the expression pattern of a comprehensive panel of TSGs and the epigenetic modifications, particularly methylation of their regulatory sequences. EBV infection of primary B lymphocytes resulted in global transcriptional repression of TSGs through engagement of hypermethylation. Therefore, CpG methylation profiles of TSGs may be used as a prognostic marker as well as development of potential therapeutic strategies for controlling acute infection and EBV-associated B-cell lymphomas. SN - 1091-6490 UR - https://www.unboundmedicine.com/medline/citation/26324942/Epigenetic_silencing_of_tumor_suppressor_genes_during_in_vitro_Epstein_Barr_virus_infection_ L2 - http://www.pnas.org/cgi/pmidlookup?view=long&pmid=26324942 DB - PRIME DP - Unbound Medicine ER -