Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic repression via DNA methylation and trimethylation of H3K27 alters gene expression in esophageal adenocarcinoma

ABSTRACT: Epigenetic repression via DNA methylation and trimethylation of H3K27 alters gene expression in esophageal adenocarcinoma

PROVIDER: PRJNA371451 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5228160.fastq.gz	Fastqsanger.gz
	SRR5228161.fastq.gz	Fastqsanger.gz
	SRR5228156.fastq.gz	Fastqsanger.gz
	SRR5228157.fastq.gz	Fastqsanger.gz
	SRR5228158.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Epigenetic repression via DNA methylation and trimethylation of H3K27 alters gene expression in esophageal adenocarcinoma [ChIP-Seq]

Project description:Epigenetic modifications in the form of altered DNA or histone methylation can influence gene expression patterns critical for neoplastic initiation and progression. The fact that abnormal gene expression can be driven by epigenetic alterations led us to examine the correlation between DNA methylation, trimethylation of histone 3 lysine 9 (H3K9me3) and lysine 27 (H3K27me3), and gene expression in esophageal adenocarcinoma (EAC). Using genome-wide approaches (chromatin immunoprecipitation/sequencing (ChIP-Seq) and methylation arrays), we identified gene targets that were enriched with the chromatin-repressive marks H3K9me3, H3K27me3, and/or DNA hypermethylation across patients with EAC. Using RNA-Seq, we found genes involved in cellular morphology and movement, epithelial cell differentiation, epithelial junction signaling, as well as genes involved in epithelial-mesenchymal transition (EMT) were down-regulated in patients with poorly differentiated EAC. Additionally, comparative analyses of ChIP-Seq, DNA methylation, and RNA-Seq data allowed us to identify a group of genes downregulated in EAC is associated with aberrant H3K27me3 enrichment or a combination of H3K27me3 and DNA hypermethylation in the poorly differentiated EAC cases. Furthermore, by comparison to TCGA data sets, H3K27me3 enrichment is associated with aberrant DNA methylation across numerous EAC cases, suggesting that dysregulation of H3K27me3 and DNA methylation is crucial in the pathogenesis of EAC.

2019-02-01 | GSE94487 | GEO

Epigenetic repression via DNA methylation and trimethylation of H3K27 alters gene expression in esophageal adenocarcinoma [RNA-Seq]

2019-02-01 | GSE94544 | GEO

H3K27 trimethylation in mouse peripheral nerve

Project description:ChIP-seq of H3K27 trimethylation in sciatic nerve H3K27me3 ChIP-Seq with corresponding input

2015-04-01 | E-GEOD-64260 | biostudies-arrayexpress

H3K27 trimethylation in mouse peripheral nerve

Project description:ChIP-seq of H3K27 trimethylation in sciatic nerve

2015-04-01 | GSE64260 | GEO

Epigenetic repression via DNA methylation and trimethylation of H3K27 alters gene expression in esophageal adenocarcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-01 | GSE94545 | GEO

Examine the impact of insulin suppression on embryo H3K27 trimethylation.

Project description:Examine the impact of insulin suppression on embryo H3K27 trimethylation.

| PRJNA661095 | ENA

Esophageal adenocarcinoma

Project description:Esophageal adenocarcinoma

| PRJNA1072671 | ENA

Esophageal Adenocarcinoma

Project description:Esophageal Adenocarcinoma

| PRJNA188928 | ENA

Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5

Project description:Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5

2013-11-11 | E-MTAB-2004 | biostudies-arrayexpress

Effect of androgen receptor signaling on H3K27 trimethylation in Th17 cells

Project description:Effect of androgen receptor signaling on H3K27 trimethylation in Th17 cells

| PRJNA1010188 | ENA