Histone H3 Lysine4 Acetylation-Methylation Dynamics Define Breast Cancer Subtypes
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ABSTRACT:
PROVIDER: PRJNA302664 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2044720.fastq.gz | Fastqsanger.gz | |||
| SRR2044730.fastq.gz | Fastqsanger.gz | |||
| SRR2044721.fastq.gz | Fastqsanger.gz | |||
| SRR2044731.fastq.gz | Fastqsanger.gz | |||
| SRR2044722.fastq.gz | Fastqsanger.gz |
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Project description:The onset and progression of breast cancer are linked to genetic and epigenetic changes that alter the normal programming of cells. Epigenetic modifications of DNA and histones contribute to chromatin structure that results in the activation or repression of gene expression. Several epigenetic pathways have been shown to be highly deregulated in cancer cells. Targeting specific histone modifications represents a viable strategy to prevent oncogenic transformation, tumor growth or metastasis. Methylation of histone H3 lysine 4 has been extensively studied and shown to mark genes for expression; however this residue can also be acetylated and the specific function of this alteration is less well known. To define the relative roles of histone H3 methylation (H3K4me3) and acetylation (H3K4ac) in breast cancer, we determined genomic regions enriched for both marks in normal-like (MCF10A), transformed (MCF7) and metastatic (MDA-MB-231) cells using a genome-wide ChIP-Seq approach. Our data revealed a genome-wide gain of H3K4ac associated with both early and late breast cancer cell phenotypes, while gain of H3K4me3 was predominantly associated with late stage cancer cells. Enrichment of H3K4ac was overrepresented at promoters of genes associated with cancer-related phenotypic traits, such as estrogen response and epithelial-to-mesenchymal transition pathways. Our findings highlight an important role for H3K4ac in predicting epigenetic changes associated with early stages of transformation. In addition, our data provide a valuable resource for understanding epigenetic signatures that correlate with known breast cancer-associated oncogenic pathways. RNA-Seq of cell lines MCF10A, MCF7 and MDA-MB-231.
2016-02-10 | E-GEOD-75168 | biostudies-arrayexpress
Project description:The onset and progression of breast cancer are linked to genetic and epigenetic changes that alter the normal programming of cells. Epigenetic modifications of DNA and histones contribute to chromatin structure that results in the activation or repression of gene expression. Several epigenetic pathways have been shown to be highly deregulated in cancer cells. Targeting specific histone modifications represents a viable strategy to prevent oncogenic transformation, tumor growth or metastasis. Methylation of histone H3 lysine 4 has been extensively studied and shown to mark genes for expression; however this residue can also be acetylated and the specific function of this alteration is less well known. To define the relative roles of histone H3 methylation (H3K4me3) and acetylation (H3K4ac) in breast cancer, we determined genomic regions enriched for both marks in normal-like (MCF10A), transformed (MCF7) and metastatic (MDA-MB-231) cells using a genome-wide ChIP-Seq approach. Our data revealed a genome-wide gain of H3K4ac associated with both early and late breast cancer cell phenotypes, while gain of H3K4me3 was predominantly associated with late stage cancer cells. Enrichment of H3K4ac was overrepresented at promoters of genes associated with cancer-related phenotypic traits, such as estrogen response and epithelial-to-mesenchymal transition pathways. Our findings highlight an important role for H3K4ac in predicting epigenetic changes associated with early stages of transformation. In addition, our data provide a valuable resource for understanding epigenetic signatures that correlate with known breast cancer-associated oncogenic pathways.
2016-02-10 | GSE75168 | GEO
Project description:The molecular signature at histone H3K4 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3 and H3K4ac histone modification associated with active chromatin to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes. H3K4me3 and H3K4ac histone modification study in normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology
2016-02-10 | E-GEOD-69377 | biostudies-arrayexpress
Project description:Histone H3 Lysine4 Acetylation-Methylation Dynamics Define Breast Cancer Subtypes [ChIP-seq]
| PRJNA285330 | ENA
Project description:The onset and progression of breast cancer are linked to genetic and epigenetic changes that alter the normal programming of cells. Epigenetic modifications of DNA and histones contribute to chromatin structure that result in the activation or repression of gene expression. Several epigenetic pathways have been shown to be highly deregulated in cancer cells. Targeting specific histone modifications represents a viable strategy to prevent oncogenic transformation, tumor growth or metastasis. Methylation of histone H3 lysine 4 has been extensively studied and shown to mark genes for expression; however this residue can also be acetylated and the specific function of this alteration is less well known. To define the relative roles of histone H3 methylation (H3K4me3) and acetylation (H3K4ac) in breast cancer, we determined genomic regions enriched for both marks in normal-like (MCF10A), transformed (MCF7) and metastatic (MDA-MB-231) cells using a genome-wide ChIP-Seq approach. Our data revealed a genome-wide gain of H3K4ac associated with both early and late breast cancer cell phenotypes, while gain of H3K4me3 was predominantly associated with late stage cancer cells. Enrichment of H3K4ac was over-represented at promoters of genes associated with cancer-related phenotypic traits, such as estrogen response and epithelial-to-mesenchymal transition pathways. Our findings highlight an important role for H3K4ac in predicting epigenetic changes associated with early stages of transformation. In addition, our data provide a valuable resource for understanding epigenetic signatures that correlate with known breast cancer-associated oncogenic pathways.
| S-EPMC4868673 | biostudies-literature
Project description:The molecular signature at histone H3K4 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3 and H3K4ac histone modification associated with active chromatin to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes.
2016-02-10 | GSE69377 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-02-10 | E-GEOD-75169 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-02-10 | GSE75169 | GEO
Project description:Normal cell type specific histone H3 acetylation of miRNA genes. HMEC and HMF represent two distinct differentiated cell type present in mammary gland each with a distinct phenotype, a distinct epigenotype as well as distinct miRNA expression pattern. The aim of the study was to determine how epigenetic modifications including histone H3 acetylation affect miRNA expression. Two cell types HMEC vs. HMF. Biological replicates: 3 pairs of HMEC-HMF of 3 distinct genotypes. Immunoprecipitation using anti-acetylated histone H3 antibody (06-599, Millipore).
2011-04-05 | E-GEOD-28375 | biostudies-arrayexpress
Project description:Histone modifications are associated with meiotic recombination hotspots, discrete sites with augmented recombination frequency. For example, trimethylation of histone H3 lysine4 (H3K4me3) marks most hotspots in budding yeast and mouse. Modified histones are known to regulate meiotic recombination partly by promoting DNA double strand break (DSB) formation, but the role and precise landscape of histone modifications at hotspots remain unclear. Here, we studied hotspot-associated modifications in fission yeast and found general features: acetylation of H3 lysine9 (H3K9ac) is strikingly elevated, and H3K4me3 is not significantly enriched. Remarkably, elimination of H3K9ac reduced binding of the DSB-inducing enzyme Rec12 and DSB at hotspots. We also found that the H3K4 metyltransferase Set1 promotes DSB formation at some loci, but it restricts Rec12 binding to hotspots. These results suggest that H3K9ac rather than H3K4me3 is a hotspot-associated mark involved in meiotic DSB formation in fission yeast.
2013-03-07 | GSE31648 | GEO