Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Increased chronic lymphocytic leukemia proliferation upon IgM stimulation is sustained by the upregulation of miR-132 and miR-212

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Teresa Colombo

PROVIDER: E-GEOD-49697 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Increased chronic lymphocytic leukemia proliferation upon IgM stimulation is sustained by the upregulation of miR-132 and miR-212.

Tavolaro Simona S Colombo Teresa T Chiaretti Sabina S Peragine Nadia N Fulci Valerio V Ricciardi Maria R MR Messina Monica M Bonina Silvia S Brugnoletti Fulvia F Marinelli Marilisa M Di Maio Valeria V Mauro Francesca R FR Del Giudice Ilaria I Macino Giuseppe G Foà Robin R Guarini Anna A

Genes, chromosomes & cancer 20150202 4

To assess the involvement of microRNAs (miRNAs) in B-cell receptor (BCR) stimulation, we first evaluated miRNA profiling following IgM cross-linking in chronic lymphocytic leukemia (CLL) cells and in normal B lymphocytes. Second, we combined miRNA and gene expression data to identify putative miRNA functional networks. miRNA profiling showed distinctive patterns of regulation after stimulation in leukemic versus normal B lymphocytes and identified a differential responsiveness to BCR engagement ...[more]

PMID: 25645730

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Project description:This is one of expressional parts of the study. These data were correlated to epigenetic changes and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively. To elucidate how a loss of DNA methylation affects a gene expression and epigenome we studied colon cancer cell line HCT116 and its derivative, HCT116 DNMT1-/- DNMT3b -/- (HCT116-DKO). According to previous studies HCT116-DKO is characterized by 95% of loss of DNA methylation. In HCT116 and HCT116-DKO cells, we profiled diverse epigenetic marks and gene expression. Further a crosstalk between epigenetic changes and transcriptional changes was analyzed. This is the expressional part of study.

Dataset Information

Increased chronic lymphocytic leukemia proliferation upon IgM stimulation is sustained by the upregulation of miR-132 and miR-212

Publications

Increased chronic lymphocytic leukemia proliferation upon IgM stimulation is sustained by the upregulation of miR-132 and miR-212.

Similar Datasets

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