ArticleBMC cancer2012
Methylation profiling of Epstein-Barr virus immediate-early gene promoters, BZLF1 and BRLF1 in tumors of epithelial, NK- and B-cell origins.
Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 43 citations in OpenAlex.
- E2F1 suppresses Epstein-Barr virus lytic reactivation through cellular and viral transcriptional networks.PLoS pathogens · 2025Article
- Review
- Review
- Epigenetic control of the Epstein-Barr lifecycle.Current opinion in virology · 2022Review
- Adoptive T-Cell Therapy for Epstein-Barr Virus-Related Lymphomas.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021Review
- Epstein-Barr Virus Promotes B Cell Lymphomas by Manipulating the Host Epigenetic Machinery.Cancers · 2020Review
- Epigenetic aberrations in natural killer/T-cell lymphoma: diagnostic, prognostic and therapeutic implications.Therapeutic advances in medical oncology · 2020Review
- Coordinate Regulation of TET2 and EBNA2 Controls the DNA Methylation State of Latent Epstein-Barr Virus.Journal of virology · 2017Article
- Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis.Biomolecules · 2016Review
- ERK/c-Jun Recruits Tet1 to Induce Zta Expression and Epstein-Barr Virus Reactivation through DNA Demethylation.Scientific reports · 2016Article
- Differentiation-Dependent KLF4 Expression Promotes Lytic Epstein-Barr Virus Infection in Epithelial Cells.PLoS pathogens · 2015Article
- Genomic assays for Epstein-Barr virus-positive gastric adenocarcinoma.Experimental & molecular medicine · 2015Review
- Genome-wide DNA methylation as an epigenetic consequence of Epstein-Barr virus infection of immortalized keratinocytes.Journal of virology · 2014Article
- Contribution of myocyte enhancer factor 2 family transcription factors to BZLF1 expression in Epstein-Barr virus reactivation from latency.Journal of virology · 2013Article
- Epigenetic modification of the Epstein-Barr virus BZLF1 promoter regulates viral reactivation from latency.Frontiers in genetics · 2013Article
- Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpstein-Barr virus (EBV) establishes its latency in EBV-associated malignancies, accompanied by occasionally reactivated lytic cycle. Promoter CpG methylation of EBV genome plays an essential role in maintaining viral latency. Two immediate-early (IE) genes, BZLF1 and BRLF1, induce the switch from latent to lytic infection. Studies of methylation-dependent binding of BZLF1 and BRLF1 to EBV promoters have been well reported, but little is known about the methylation status of BZLF1 and BRLF1 promoters (Zp and Rp) in tumor samples.
methodsWe evaluated the methylation profiles of Zp and Rp by methylation-specific PCR (MSP) and bisulfite genomic sequencing (BGS), as well as BZLF1 and BRLF1 expression by semiquantitative reverse transcription (RT)-PCR in tumors of epithelial, NK- and B-cell origins.
resultsWe found that both Zp and Rp were hypermethylated in all studied EBV-positive cell lines and tumors of lymphoid (B- or NK cell) or epithelial origin, while unmethylated Zp and Rp alleles were detected in cell lines expressing BZLF1 and BRLF1. Following azacytidine treatment or combined with trichostatin A (TSA), the expression of BZLF1 and BRLF1 was restored along with concomitant promoter demethylation, which subsequently induced the reactivation of early lytic gene BHRF1 and late lytic gene BLLF1.
conclusionsHypermethylation of Zp and Rp mediates the frequent silencing of BZLF1 and BRLF1 in EBV-associated tumors, which could be reactivated by demethylation agent and ultimately initiated the EBV lytic cascade.
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