Differential DNA methylation profiles of human B lymphocytes and Epstein-Barr virus-immortalized B lymphocytes

Zhang, Chaoting; Zhang, Rui; Chen, Zhiqiang; Chen, Jing; Ruan, Jigang; Zhang, Lu; Xiong, Hongchao; Yang, Wenjun

doi:10.21147/j.issn.1000-9604.2018.01.11

Cited by 10 publications

(9 citation statements)

References 26 publications

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“…This study reports a comparison of the data generated by Illumina's Infinium MethylationEPIC BeadChip array technology for gDNA from peripheral blood leukocytes from 16 individuals and clDNA, derived from EBV transformation of the same samples into cell lines performed by the ECACC. The methylationEPIC BeadChip array covers 862,927 CpG sites, which makes this the largest gDNA and clDNA methylation profiling study using this array [15]. DNA methylation plays a key role in epigenetic gene regulation and is the most well studied epigenetic factor [16].…”

Section: Discussionmentioning

confidence: 99%

Comparison of methylation patterns generated from genomic and cell-line derived DNA using the Illumina Infinium MethylationEPIC BeadChip array

et al. 2019

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Objectives: Genomic DNA (gDNA) is the optimal source of DNA for methylation analysis. This study compared methylation patterns in gDNA derived from blood with cell-line derived DNA (clDNA) from the same individuals. The clDNA had been generated via an Epstein-Barr virus transformation of the participant's lymphocytes. This analysis sought to determine whether clDNA has the potential to be utilised in lieu of finite/unavailable gDNA in methylation analyses using Illumina Infinium MethylationEPIC BeadChip arrays that assess 862,927 CpG sites. Results: DNA samples were divided into two groups with eight gDNA and eight matched clDNA samples compared in each group (n = 16 individuals with 32 samples in total). Methylation patterns for gDNA samples generated for both groups were compared to the clDNA equivalent samples using Partek ® Genomics Suite ® to assess whether the significantly different CpG sites were consistent between both groups. In total, 28,632 CpG sites with significantly different levels of methylation (p < ×10 −8) were common to both groups while 828,072 CpG sites assessed by the MethylationEPIC array were not significantly different in either group. This indicates that there is potential for clDNA to be used as a replacement for finite gDNA samples when absolutely necessary in DNA methylation studies.

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Section: Discussionmentioning

confidence: 99%

Comparison of methylation patterns generated from genomic and cell-line derived DNA using the Illumina Infinium MethylationEPIC BeadChip array

et al. 2019

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“…hypermethylation phenotype in EBV-transformed B cells is not frequently observed (18,69,70), notable methylation patterns in some key TSGs are evident (71). By comparing peripheral primary B cells and the corresponding EBV-transformed B cells, Saha and colleagues showed that EBV infection resulted in four methylation patterns for the TSGs, namely gain of methylation, loss of methylation, distinct methylation, and fluctuating methylation (71).…”

Section: Ebv Transformation Of B Cells Is Associated With Hypomethylamentioning

confidence: 99%

The Impact of Epstein-Barr Virus Infection on Epigenetic Regulation of Host Cell Gene Expression in Epithelial and Lymphocytic Malignancies

Leong

Lung

2021

Front. Oncol.

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Epstein-Barr virus (EBV) infection is associated with a variety of malignancies including Burkitt’s lymphoma (BL), Hodgkin’s disease, T cell lymphoma, nasopharyngeal carcinoma (NPC), and ∼10% of cases of gastric cancer (EBVaGC). Disruption of epigenetic regulation in the expression of tumor suppressor genes or oncogenes has been considered as one of the important mechanisms for carcinogenesis. Global hypermethylation is a distinct feature in NPC and EBVaGC, whereas global reduction of H3K27me3 is more prevalent in EBVaGC and EBV-transformed lymphoblastoid cells. In BL, EBV may even usurp the host factors to epigenetically regulate its own viral gene expression to restrict latency and lytic switch, resulting in evasion of immunosurveillance. Furthermore, in BL and EBVaGC, the interaction between the EBV episome and the host genome is evident with respectively unique epigenetic features. While the interaction is associated with suppression of gene expression in BL, the corresponding activity in EBVaGC is linked to activation of gene expression. As EBV establishes a unique latency program in these cancer types, it is possible that EBV utilizes different latency proteins to hijack the epigenetic modulators in the host cells for pathogenesis. Since epigenetic regulation of gene expression is reversible, understanding the precise mechanisms about how EBV dysregulates the epigenetic mechanisms enables us to identify the potential targets for epigenetic therapies. This review summarizes the currently available epigenetic profiles of several well-studied EBV-associated cancers and the relevant distinct mechanisms leading to aberrant epigenetic signatures due to EBV.

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“…This observation was supported by an independent study where the top susceptibility variants for BD were found to be enriched in mQTLs in the cerebellum, but not in transformed lymphocytes ( 90 ). However, as the transformation alters the methylomic landscape of cells, it is unclear how this process impacts methylation levels at mQTL loci and further detection of the enrichment ( 91 ). Candidate gene study of BD risk SNPs in CACNA1C confirmed its risk variants to act as cis- mQTLs in blood ( 92 ).…”

Section: Evidence For the Impact Of Methylation Quantitative Trait Lomentioning

confidence: 99%

Role of DNA Methylation in Mediating Genetic Risk of Psychiatric Disorders

Starnawska

Demontis

2021

Front. Psychiatry

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Psychiatric disorders are common, complex, and heritable conditions estimated to be the leading cause of disability worldwide. The last decade of research in genomics of psychiatry, performed by multinational, and multicenter collaborative efforts on hundreds of thousands of mental disorder cases and controls, provided invaluable insight into the genetic risk variants of these conditions. With increasing cohort sizes, more risk variants are predicted to be identified in the near future, but there appears to be a knowledge gap in understanding how these variants contribute to the pathophysiology of psychiatric disorders. Majority of the identified common risk single-nucleotide polymorphisms (SNPs) are non-coding but are enriched in regulatory regions of the genome. It is therefore of great interest to study the impact of identified psychiatric disorders' risk SNPs on DNA methylation, the best studied epigenetic modification, playing a pivotal role in the regulation of transcriptomic processes, brain development, and functioning. This work outlines the mechanisms through which risk SNPs can impact DNA methylation levels and provides a summary of current evidence on the role of DNA methylation in mediating the genetic risk of psychiatric disorders.

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Differential DNA methylation profiles of human B lymphocytes and Epstein-Barr virus-immortalized B lymphocytes

Abstract: Our study demonstrated genome-wide DNA methylation variations between primary B cells and corresponding LCLs, which might yield new insight on the methylation mechanism of EBV-induced immortalization.

Cited by 10 publications

References 26 publications

Comparison of methylation patterns generated from genomic and cell-line derived DNA using the Illumina Infinium MethylationEPIC BeadChip array

Comparison of methylation patterns generated from genomic and cell-line derived DNA using the Illumina Infinium MethylationEPIC BeadChip array

The Impact of Epstein-Barr Virus Infection on Epigenetic Regulation of Host Cell Gene Expression in Epithelial and Lymphocytic Malignancies

Role of DNA Methylation in Mediating Genetic Risk of Psychiatric Disorders

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