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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC [ATAC-seq]

ABSTRACT: Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC [ATAC-seq]

PROVIDER: PRJNA1071124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27788500_1.fastq.gz	Fastqsanger.gz
	SRR27788500_2.fastq.gz	Fastqsanger.gz
	SRR27788501_1.fastq.gz	Fastqsanger.gz
	SRR27788501_2.fastq.gz	Fastqsanger.gz
	SRR27788502_1.fastq.gz	Fastqsanger.gz

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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. [ChIP-Seq]

Project description:BRAFV600E-mutated colorectal cancer (CRC) exhibits a strong correlation with DNA hypermethylation suggesting this subgroup of tumors is uniquely presenting epigenomic phenotypes. Nonetheless, the traditional epigenomic therapeutic agent, 5-azacitidine, which inhibits DNA methyltransferase activity, did not yield sufficient improvements in the efficacies of BRAFV600E CRC in vivo. We utilized a patient-derived xenograft model and confirmed an effective reduction of DNA methylation levels upon 5-azacitidine treatment yet failed to restore gene expression patterns. This study unbiasedly explored the adaptive engagement of other epigenomic modifications upon the profound decrease in DNA methylation by azacitidine treatment. A loss of histone acetylation and a gain of histone methylations, including H3K27 and H3K4 trimethylation, were observed around hypomethylated regions. Our findings suggested a compensatory increase in repressive histone mark, H3K27 trimethylation, around treatment-induced hypomethylated regions, which suggests the involvement of polycomb repressive complex (PRC) activity around the genome with lost DNA methylation, therefore maintaining the suppression of key genes. Combined inhibition of PRC activity through EZH2 inhibitor with azacitidine treatment additively improved efficacies in BRAFV600E CRC cells. In conclusion, DNA hypermethylation exhibits a close association with H3K27me3 and PRC activity in BRAFV600E CRC, and simultaneous blockade of DNMT and EZH2 holds promise as a potential therapeutic strategy for patients with BRAFV600E-mutated CRC.

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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC [ATAC-seq]

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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. [RNA-Seq]

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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC.

Project description:Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC.

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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. [ChIP-Seq]

Project description:Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. [ChIP-Seq]

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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. [RNA-Seq]

Project description:Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. [RNA-Seq]

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H3K27 trimethylation in mouse peripheral nerve

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Mapping of H3K4 and H3K27 trimethylation in zebrafish cells (ChIP-chip)

Project description:The genomic distribution of post-translationally modified histones in the zebrafish (Danio rerio) genome remain largely unraveled. The objective of this study was to (1) design a microarray covering all zebrafish gene promoters and 5' end of coding regions, and (ii) using these arrrays, map the genome-wide distribution of trimethylated H3K4 and H3K27 in the mbryo derived ZF4 cell line. Specifically, we determined teh enrichment profile of H3K4me3, H3K27me3 and of both (co-enriched) modifications in ZF4 cells. We determined average enrichment profiles through metagene analysis, functional terms enriched among genes marked by either modification, and pathway analysis. ChIP-chip experiments were performed from duplicate cultures

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Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC.

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

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