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DNA methylation prevents CTCF-mediated silencing of the oncogene BCL6 in B cell lymphomas

ABSTRACT: Elevated DNA methylation in the first intronic region of the BCL6 locus in B cell lymphomas enforces transcription of the BCL6 gene Promoter tiling arrays were used to investigate the distribution of DNA methylation near the promoter region of BCL6 locus

ORGANISM(S): Homo sapiens

PROVIDER: GSE22884 | GEO | 2010/08/20

SECONDARY ACCESSION(S): PRJNA128141

REPOSITORIES: GEO

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DNA methylation prevents CTCF-mediated silencing of the oncogene BCL6 in B cell lymphomas

Project description:Elevated DNA methylation in the first intronic region of the BCL6 locus in B cell lymphomas enforces transcription of the BCL6 gene Promoter tiling arrays were used to investigate the distribution of DNA methylation near the promoter region of BCL6 locus Comparison of DNA methylation at promoter regions of lymphoma (Raji) and myeloma (H929) cell lines by methylated CpG island recovery assay (MIRA-chip)

2010-08-20 | E-GEOD-22884 | biostudies-arrayexpress

BCL6-centric reorganization of the genome during B cell affinity maturation

Project description:During the humoral immune response mature B-cells undergo a dramatic change in phenotype to enable antibody affinity maturation in germinal centers (GCs). Here, we observe for the first time that these phenotypic changes are accompanied by large-scale reorganization of the genomic architecture that encodes the GCB-cell transcriptional program. The coordinate expression of genes that specify the GCB-cell phenotype – most prominently, BCL6 – is achieved through a non-random, multilayered, chromatin reorganization process involving i) increased promoter connectivity, ii) formation of higher-order enhancer networks, iii) 5’ to 3’ gene looping, and iv) merging of gene neighborhoods that share active epigenetic marks. These cell-specific events are closely linked to binding of GC transcription factors and the structural proteins CTCF and cohesin. The gene encoding the GC master regulator, BCL6, is an anchor point for the formation of GC-specific gene and enhancer loops on chromosome 3. Furthermore, through CRISPR-mediated knockout we demonstrate that a putative locus control region upstream of Bcl6 is required for GCB-cell formation in mice. Thus, architectural reorganization of phenotype-driving gene sets, including assembly of cell type-specific promoter and enhancer networks, may be key to controlling tissue-specific gene expression programs.

2016-09-26 | GSE84022 | GEO

DNA methylation prevents CTCF-mediated silencing of the oncogene BCL6 in B cell lymphomas.

Project description:Aberrant DNA methylation commonly occurs in cancer cells where it has been implicated in the epigenetic silencing of tumor suppressor genes. Additional roles for DNA methylation, such as transcriptional activation, have been predicted but have yet to be clearly demonstrated. The BCL6 oncogene is implicated in the pathogenesis of germinal center-derived B cell lymphomas. We demonstrate that the intragenic CpG islands within the first intron of the human BCL6 locus were hypermethylated in lymphoma cells that expressed high amounts of BCL6 messenger RNA (mRNA). Inhibition of DNA methyltransferases decreased BCL6 mRNA abundance, suggesting a role for these methylated CpGs in positively regulating BCL6 transcription. The enhancer-blocking transcription factor CTCF bound to this intronic region in a methylation-sensitive manner. Depletion of CTCF by short hairpin RNA in neoplastic plasma cells that do not express BCL6 resulted in up-regulation of BCL6 transcription. These data indicate that BCL6 expression is maintained during lymphomagenesis in part through DNA methylation that prevents CTCF-mediated silencing.

| S-EPMC2931164 | biostudies-literature

Bcl6

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