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ChIP-seq of H3K27ac and H3K27me3 in HSJD-DIPG-007 cell line

ABSTRACT: ChIP-seq of H3K27ac and H3K27me3 in HSJD-DIPG-007 cell line

PROVIDER: PRJEB33970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3477250.fastq.gz	Fastqsanger.gz
	ERR3477251.fastq.gz	Fastqsanger.gz
	ERR3477252.fastq.gz	Fastqsanger.gz
	ERR3477253.fastq.gz	Fastqsanger.gz
	ERR3477246.fastq.gz	Fastqsanger.gz

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ChIP-seq of H3K27ac and H3K27me3 in HSJD-DIPG-007 cell line

Project description:Identification of super enhancer regions in the HSJD-DIPG-007 cell line and the associated genes with these regions. This study aims to evaluate the efficacy of combined use of BET and CBP inhibition in DIPG.

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ChIP-seq of H3K27ac and H3K27me3 in HSJD-DIPG-007 cell line upon treatment with ICG-001 and JQ1

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ChIP-seq of H3K27ac and H3K27me3 in HSJD-DIPG-007 cell line upon treatment with ICG-001 and JQ1

Project description:ChIP-seq of H3K27ac and H3K27me3 in HSJD-DIPG-007 cell line upon treatment with ICG-001 and JQ1

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PRMT5 inhibition by LLY-283 in HSJD-DIPG-007 DMG cells

Project description:H3K27-altered Diffuse Midline Glioma (DMG) is a universally fatal paediatric brainstem tumour. The prevalent driver mutation H3K27M creates a unique epigenetic landscape that may also establish therapeutic vulnerabilities to epigenetic inhibitors. From a wider screen of an epigenetic inhibitor library, we identified PRMT5 inhibitors as amongst the top hits reducing DMG cell viability. Here, we treated HSJD-DIPG-007 +/- the PRMT5 inhibitor LLY-283. RNA-sequencing was performed at 0, 1, 2, 3, 5, 7 and 10 days to assess the changes in gene expression following PRMT5 inhibition in DMG cells. This shows that PRMT5 inhibition changes expression in genes associated with multiple disease relevant phenotypes, including sterol metabolism, differentiation, and the extracellular matrix. By characterising the changes in the transcriptome following PRMT5 inhibition this provides crucial insights into the potential of PRMT5 inhibitors as a treatment for H3K27-altered DMG.

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PRMT5 inhibition by LLY-283 in HSJD-DIPG-007 DMG cells

Project description:PRMT5 inhibition by LLY-283 in HSJD-DIPG-007 DMG cells

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Heterotypic nucleosomes and PRC2 drive DIPG oncogenesis

Project description:Diffuse intrinsic pontine gliomas (DIPG) are characterized by a heterozygous lysine-to-methionine mutation of histone H3 (H3K27M) that potently reduces Polycomb Repressive Complex 2 (PRC2) methylation of wild-type histone H3K27 (H3K27wt). The role of H3K27M and reduced H3K27wt methylation in DIPG pathogenesis has yet to be determined. Here, we have performed epigenomic profiling of patient-derived H3K27M mutant DIPG cells and demonstrate that H3K27M resides in nucleosomes with H3K27wt acetylation (H3K27ac), and H3K27M-H3K27ac containing nucleosomes co-localize with bromodomain proteins at actively transcribed genes and that PRC2 is excluded from H3K27M occupied regions. With respect to therapeutic implications of these observations, we demonstrate that pharmacologic bromodomain protein inhibition suppresses tumor growth in vivo. In total, our results indicate that H3K27M promotes H3K27ac at the expense of H3K27 methylation, and points to bromodomain protein inhibition as a clinical strategy for treating DIPG.

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