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Epigenomic reprogramming due to PRC2 functional loss induces an aggressive de-differentiated neural crest-like phenotype in MPNST

ABSTRACT: Epigenomic reprogramming due to PRC2 functional loss induces an aggressive de-differentiated neural crest-like phenotype in MPNST

PROVIDER: PRJNA593495 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10587300.fastq.gz	Fastqsanger.gz
	SRR10587301.fastq.gz	Fastqsanger.gz
	SRR10587302.fastq.gz	Fastqsanger.gz
	SRR10587303.fastq.gz	Fastqsanger.gz
	SRR10587304.fastq.gz	Fastqsanger.gz

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Project description:In order to comprehensively define the epigenetic patterns specific to MPNST, we generated profiles for 6 histone modification marks, including H3K4me1 (enhancer), H3K27Ac (active enhancer), H3K9me3 (heterochromatin), H3K27me3 (polycomb repression), H3K79me2 (transcription) and H3K4me3 (promoter). Systematic epigenomic profiling of chromatin states in MPNST cells revealed epigenetic subtypes in MPNST based on Polycomb related repressive and bivalent chromatin states. We demonstrate that PRC2 loss led to de-repression and subsequent enhancer reprogramming at key neural crest specifiers aiding the acquisition of this de-differentiated aggressive tumor phenotype.

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