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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94487 | GEO | 2019/02/01

REPOSITORIES: GEO

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Epigenetic repression via DNA methylation and trimethylation of H3K27 alters gene expression in esophageal adenocarcinoma [RNA-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 | GSE94544 | GEO

Bisulfite sequencing of ChIP DNA on breast cancer cells (HCC1954)

Project description:While genetic mutation is a hallmark of cancer, many cancers also acquire epigenetic alterations during tumorigenesis including aberrant DNA hypermethylation of tumor suppressors as well as changes in chromatin modifications as caused by genetic mutations of the chromatin-modifying machinery. However, the extent of epigenetic alterations in cancer cells has not been fully characterized. Here, we describe the first complete methylome maps at single nucleotide resolution of a low-passage breast cancer cell line and primary human mammary epithelial cells. We find widespread DNA hypomethylation in the cancer cell, primarily at partially methylated domains (PMDs) in normal breast cells. Unexpectedly, genes within these regions are largely silenced in cancer cells. The loss of DNA methylation in these regions is accompanied by formation of repressive chromatin, with a significant fraction displaying allelic DNA methylation where one allele is DNA methylated while the other allele is occupied by histone modifications H3K9me3 or H3K27me3. Our results show a mutually exclusive and complementary relationship between DNA methylation and H3K9me3 or H3K27me3. These results suggest that global DNA hypomethylation in breast cancer is tightly linked to the formation of repressive chromatin domains and gene silencing, thus identifying a potential epigenetic pathway for gene regulation in cancer cells and suggesting a possible new approach toward the development of cancer therapeutics. ChIP-methylC-Seq on H3K9me3, H3K27me3, and H3K36me3 in breast cancer HCC1954. 36 cycles of sequencing on Illumina platform.

2011-09-16 | E-GEOD-29120 | biostudies-arrayexpress

Comparative DNA methylome analysis of endometrioid adenocarcinoma, uterine papillary serous carcinoma, and normal endometrium

Project description:Classically, there are two types of endometrial cancer, endometrioid adenocarcinoma (EAC), or Type I; and uterine papillary serous carcinoma (UPSC), or Type II. These two types of cancers exhibit distinct DNA methylation levels in promoters of many genes. In EAC, many tumor suppressor genes were silenced due to DNA hypermethylation at their promoter region. However, promoters of many of these genes remained unmethylated in UPSC. Here, we described complete DNA methylome maps of endometrioid adenocarcinoma, uterine papillary serous carcinoma, and normal endometrium, by applying a combined strategy of methylated DNA immunoprecipitation sequencing (MeDIP-seq) and methylation-sensitive restriction enzyme sequencing (MRE-seq). We took a complementary and orthogonal approach to identify DNA methylation changes unique to the two endometrial cancer subtypes in an unbiased fashion. We generated complete DNA methylome maps for endometrioid adenocarcinoma (EAC, three samples), uterine papillary serous carcinomas (UPSC, three samples), and normal endometrium (pooled samples) by integrating data from methylated DNA immunoprecipitation sequencing (MeDIP-seq) and methylation-sensitive restriction enzyme sequencing (MRE-seq).

2014-10-12 | E-GEOD-51565 | biostudies-arrayexpress

Gene expression analysis of breast cancer (HCC1954) and normal breast cells (HMEC)

Project description:While genetic mutation is a hallmark of cancer, many cancers also acquire epigenetic alterations during tumorigenesis including aberrant DNA hypermethylation of tumor suppressors as well as changes in chromatin modifications as caused by genetic mutations of the chromatin-modifying machinery. However, the extent of epigenetic alterations in cancer cells has not been fully characterized. Here, we describe the first complete methylome maps at single nucleotide resolution of a low-passage breast cancer cell line and primary human mammary epithelial cells. We find widespread DNA hypomethylation in the cancer cell, primarily at partially methylated domains (PMDs) in normal breast cells. Unexpectedly, genes within these regions are largely silenced in cancer cells. The loss of DNA methylation in these regions is accompanied by formation of repressive chromatin, with a significant fraction displaying allelic DNA methylation where one allele is DNA methylated while the other allele is occupied by histone modifications H3K9me3 or H3K27me3. Our results show a mutually exclusive and complementary relationship between DNA methylation and H3K9me3 or H3K27me3. These results suggest that global DNA hypomethylation in breast cancer is tightly linked to the formation of repressive chromatin domains and gene silencing, thus identifying a potential epigenetic pathway for gene regulation in cancer cells and suggesting a possible new approach toward the development of cancer therapeutics. mRNA-Seq of polyA-selected RNA from breast cancer HCC1954 and normal breast HMEC. 36 cycles of sequencing on Illumina platform.

2011-09-16 | E-GEOD-29119 | biostudies-arrayexpress

Comparative DNA methylome analysis of endometrioid adenocarcinoma, uterine papillary serous carcinoma, and normal endometrium

2014-10-12 | GSE51565 | GEO

Examining the effect of the linker DNA length on protein binding to di-nucleosomes decorated with H3K9me3 and H3K27me3

Project description:Characteristic features of chromatin states are not limited to particular epigenetic modifications but include other regulatory cues, such as linker DNA length, typically ranging from between 35-55 bp (Valouev et al, 2011; Voong et al., 2016, Cell) to over 200 bp in nucleosome-depleted regions (NDRs) found at active enhancers and promoters (Schones et al, 2008; Hansen He et al, 2010). To investigate whether and how the nucleosome linker DNA affects chromatin recognition by nuclear proteins we performed a set of affinity purifications using di-nucleosomes incorporating different DNA linkers. This dataset contains experiments aimed to probe how the linker DNA length affects protein binding to di-nucleosomes decorated with H3K9me3 or H3K27me3. The following di-nucleosomes were used in affinity pull-down purifications with HeLa nuclear extract followed by label-free MS: 1. unmod. H3, 35 bp linker 2. unmod. H3, 40 bp linker 3. unmod. H3, 45 bp linker 4. unmod. H3, 50 bp linker 5. unmod. H3, 55 bp linker 6. H3K9me3, 35 bp linker 7. H3K9me3, 40 bp linker 8. H3K9me3, 45 bp linker 9. H3K9me3 50 bp linker 10. H3K9me3, 55 bp linker 11. H3K27me3, 35 bp linker 12. H3K27me3, 40 bp linker 13. H3K27me3, 45 bp linker 14. H3K27me3, 50 bp linker 15. H3K27me3, 55 bp linker

2023-12-10 | PXD042368 | Pride

An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells (WGBS)

Project description:DNA methylation profoundly impacts genome regulation, notably through the control of transposons. DNA methylation is extensively remodeled during two developmental periods in mammals, gametogenesis and early embryogenesis. Most of transposons families become then hypomethylated, raising the question of their regulation in absence of DNA methylation. To induce genome-wide demethylation, we relied on hypomethylation-inducing culture conditions of murine embryonic stem cells. Surprisingly, we observed two phases of transposon regulation. After a burst of derepression, which correlates with DNA methylation disappearance, both LTR and non-LTR retrotransposons were efficiently re-silenced. While histone H3 lysine 9 trimethylation (H3K9me3) remained stable, H3 lysine 27 trimethylation (H3K27me3) was reorganized upon loss of DNA methylation and contributed to transposon re-silencing. Interestingly, we observed that H3K9me3 and H3K27me3 co-occurred but in distinct regions of unmethylated transposon sequences. This unusual pattern may provide a mechanistic relay ensuring genome stability during developmental periods of programmed loss of DNA methylation.

2016-01-27 | GSE71592 | GEO

An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells (ChIP-Seq)

2016-01-27 | GSE71589 | GEO

An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells (RNA-Seq)

2016-01-27 | GSE71591 | GEO

Genome-wide maps of chromatin histone methylation marks in neonatal and adult cardiomyocytes

Project description:Epigenetic changes in DNA and chromatin are implicated in organogenesis and cell differentiation. Through a genome-wide chromatin-immunoprecipitation DNA-sequencing approach (ChIP-seq) we analyses the enrichment of H3K79me2 and H3K4me3 (histone methylation marks associated with transcriptional activation) and H3K27me3 and H3K9me3 (histone methylation marks associated with transcriptional repression) in neonatal and adult cardiomyocytes. The histone methylation profile obtained was correlated with an Illumina gene expression profile from the same samples. Our results demonstrate that histone methylation, and in particular the DOT1L-mediated H3K79me2 mark, drives cardiomyogenesis through the definition of a specific transcriptional landscape Profiling of H3K79me2, H3K4me3, H3K27me3 and H3K9me3 in neonatal and adult cardiomyocytes

2014-12-22 | E-GEOD-45174 | biostudies-arrayexpress

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