Average_hypermethylation_TF_sites
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00010002411 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Average genome-wide methylation levels per sample at different time points using nanopolish calls. Data from 8 individuals.
| EGAD00010002412 | EGA
Project description:Average methylation levels based on nanopolish calls from Roadmap Epigenomics histone mark annotations using different cell types. Data from 8 individuals at different time points.
| EGAD00010002422 | EGA
Project description:Average methylation levels based on nanopolish calls from Roadmap Epigenomics chromatin state annotations using different cell types. Data from 8 individuals at different time points.
| EGAD00010002413 | EGA
Project description:Average methylation difference 12 months vs 0 months at Roadmap Epigenomics chromatin state annotations from different cell types using nanopolish. Data from 8 individuals.
| EGAD00010002410 | EGA
Project description:Background: Epigenetic modification is a hallmark of cancer cells achieved through altered patterns of DNA methylation, histone modifications and nucleosome positions. These events have only been described in detail at gene promoters. Results: Here, we integrate multiple epigenome-wide maps to evaluate the scope of global epigenetic reprogramming in cancer cells at enhancers and insulators. Using high-resolution simultaneous mapping of global DNA methylation and nucleosome positions within individual DNA strands (NOMe-Seq), we observe a reorganization of the DNA methylome coupled with simultaneous modulation of nucleosome depleted regions (NDRs) at distal regulatory elements in cancer cells. We show that while NDRs are preferentially found at enhancers in normal breast and prostate epithelial cells, there are fewer NDRs coupled with increased DNA methylation detected at enhancersin cancer cells. Our data suggests that the acquisition of a nucleosome is key to DNA hypermethylation susceptibility and contributes to epigenetic silencing of enhancers in cancer, which can notably occur without loss of H3K4me1. Further we observe that NDRs are not necessary for peripheral phasing of adjacent nucleosomes, contrary to the common dogma, and show that nucleosomes remain organized and phased, even in the absence of a NDR as an anchor. Finally we observe the potential for transcription factors (TF) to organize NDRs genome-wide; all TF-binding sites are strongly hypomethylated and some show extensive peripheral nucleosome phasing. Conclusion: Together our findings suggest that, in addition to epigenetic alterations to promoter regions in cancer, there is substantial disruption to the distal regulatory architecture that provides an additional layer of epigenetic plasticity in malignancy. NOMe-seq, ChIP-seq for 5 marks and input control for breast normal (HMEC), breast cancer (MCF7), prostate normal (PrEC) and prostate cancer (PC3) cell lines
2014-06-04 | E-GEOD-57498 | biostudies-arrayexpress
Project description:Gene expression analysis of a CRC cell line showing wide-spread DNA hypermethylation (SW48) before and after 5-Aza-Cytidine/Trichostatin A induced DNA demethylation to identify targets of Cytosine methylation-dependent gene silencing.
2019-03-22 | GSE37873 | GEO
Project description:The impact of healthy aging on molecular programming of immune cells is poorly understood. Here, we report comprehensive characterization of healthy aging in human classical monocytes, with a focus on epigenomic, transcriptomic, and proteomic alterations, as well as the corresponding proteomic and metabolomic data for plasma, using healthy cohorts of 20 young and 20 older males (~27 and ~64 years old on average). For each individual, we performed eRRBS-based DNA methylation profiling, which allowed us to identify a set of age-associated differentially methylated regions (DMRs) – a novel, cell-type specific signature of aging in DNA methylome. Hypermethylation events were associated with H3K27me3 in the CpG islands near promoters of lowly-expressed genes, while hypomethylated DMRs were enriched in H3K4me1 marked regions and associated with age-related increase of expression of the corresponding genes, providing a link between DNA methylation and age-associated transcriptional changes in primary human cells.
2022-02-16 | PXD021821 | Pride
Project description:DNA methylation controls gene expression and is altered in many types of disease, including metastatic colorectal cancer. Studying this phenomenon in archival material such as formalin-fixed paraffin embedded (FFPE) tumour biopsies would represent a significant step in unlocking a previously unavailable source of data. Methylation at base-pair resolution has not been fully described in FFPE samples in the context of matched fresh frozen (FF) tumour material using a targeted next-generation sequencing approach. Here, we used three pairs of matched FFPE and FF samples, along with two cell lines in duplicate, to determine the extent of their similarity. We identified a “bowing” pattern in FFPE samples showing lower CpG proportion at the start of sequence reads, but found no evidence that this significantly affected methylation calls. We also found no significant increase in deamination, measured by C > T transitions, previously considered a result of cross-linking DNA by formalin fixation and a barrier to FFPE use in methylation studies. Finally, our method has shown sensitivity of between 60-70% based on positions also methylated in cell lines. This level is not affected by coverage, and we believe that FFPE material is useful as a tissue source for similar methylation studies.
2017-07-08 | GSE84171 | GEO
Project description:Background: Epigenetic modification is a hallmark of cancer cells achieved through altered patterns of DNA methylation, histone modifications and nucleosome positions. These events have only been described in detail at gene promoters. Results: Here, we integrate multiple epigenome-wide maps to evaluate the scope of global epigenetic reprogramming in cancer cells at enhancers and insulators. Using high-resolution simultaneous mapping of global DNA methylation and nucleosome positions within individual DNA strands (NOMe-Seq), we observe a reorganization of the DNA methylome coupled with simultaneous modulation of nucleosome depleted regions (NDRs) at distal regulatory elements in cancer cells. We show that while NDRs are preferentially found at enhancers in normal breast and prostate epithelial cells, there are fewer NDRs coupled with increased DNA methylation detected at enhancersin cancer cells. Our data suggests that the acquisition of a nucleosome is key to DNA hypermethylation susceptibility and contributes to epigenetic silencing of enhancers in cancer, which can notably occur without loss of H3K4me1. Further we observe that NDRs are not necessary for peripheral phasing of adjacent nucleosomes, contrary to the common dogma, and show that nucleosomes remain organized and phased, even in the absence of a NDR as an anchor. Finally we observe the potential for transcription factors (TF) to organize NDRs genome-wide; all TF-binding sites are strongly hypomethylated and some show extensive peripheral nucleosome phasing. Conclusion: Together our findings suggest that, in addition to epigenetic alterations to promoter regions in cancer, there is substantial disruption to the distal regulatory architecture that provides an additional layer of epigenetic plasticity in malignancy.
2014-06-04 | GSE57498 | GEO
Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. Enhanced Reduced Representation Bisulfite Sequencing (eRRBS) analysis of in vitro-grown hematopoietic cells transduced with AML1-ETO or MLL-AF9
2015-04-22 | E-GEOD-59584 | biostudies-arrayexpress