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The histone modification change between PRC2-wt and PRC2-loss in human MPNST cancer cells

ABSTRACT: The histone modification change between PRC2-wt and PRC2-loss in human MPNST cancer cells

PROVIDER: PRJNA836551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19146100_1.fastq.gz	Fastqsanger.gz
	SRR19146100_2.fastq.gz	Fastqsanger.gz
	SRR19146101_1.fastq.gz	Fastqsanger.gz
	SRR19146101_2.fastq.gz	Fastqsanger.gz
	SRR19146102_1.fastq.gz	Fastqsanger.gz

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The histone modification change between PRC2-wt and PRC2-loss in human MPNST cancer cells

Project description:PRC2-isogenic human malignant peripheral nerve sheath tumor (MPNST) M3 cells were generated through CRISPR/Cas9-mediated knockout of the PRC2 core component, SUZ12. PRC2 loss leads to global loss of H3K27me3, which causes H3K27ac redistribution and also affect other histone modification, e.g., H3K36me2/3.

2022-08-17 | GSE202555 | GEO

Transcriptome analysis between PRC2-loss and PRC2-wt in human malignant peripheral nerve sheath tumor (MPNST)

Project description:PRC2 loss of function occurs frequently in human MPNST. Here, we found that PRC2-loss tumors are separated from PRC2-wt ones at the transcriptome level by RNA-seq among 41 human MPNST tumor tissues.

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The chromatin accessibility change by PRC2 inactivation with or without IFNγ stimulation in human MPNST cancer cells

Project description:PRC2-isogenic human malignant peripheral nerve sheath tumor (MPNST) M3 cells were generated through CRISPR/Cas9-mediated knockout of the PRC2 core component, SUZ12. PRC2 loss led to not only significant increase, but also significant decrease of chromatin accessibility at 15,346 (16% of all ATAC peaks) and 20,099 genomic loci (21% of all ATAC peaks), respectively. PRC2 loss decreased the chromatin accessibility for IFNγ-responsive loci in M3 cells, resulting in dampened response to IFNγ stimulation.

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Transcriptome analysis between PRC2-loss and PRC2-wt in human malignant peripheral nerve sheath tumor (MPNST)

Project description:Transcriptome analysis between PRC2-loss and PRC2-wt in human malignant peripheral nerve sheath tumor (MPNST)

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PRC2 is a tumor suppressor in malignant peripheral nerve sheath tumor (MPNST)

Project description:Using mouse models, we show that PRC2 restrains MPNST development in the peripheral nervous system in the absence of both Nf1 and Cdkn2a tumor suppressor genes. Here we conducted bulk RNA-sequencing of tumors generated in mice.

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ChIP-seq dataset for epigenomic landscape of MPNST

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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RNA-seq dataset for MPNST patient tissue samples

Project description:Comprehensive transcriptomic profiling of PRC2 mutant MPNST patient tissues with adjacent normal tissues and neurofibroma patient tissues was performed to investigate gain of specific transcriptional signature associated with PRC2 loss during transformation to MPNST.

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Project description:Comprehensive transcriptomic profiling of PRC2 mutant and WT MPNST cell lines were performed to investigate PRC2-dependent transcriptional programs that are activated due to PRC2 loss

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Project description:The chromatin accessibility change by PRC2 inactivation with or without IFNγ stimulation in human MPNST cancer cells

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PRC2 loss drives MPNST metastasis and matrix remodeling.

Project description:The histone methyltransferase PRC2 plays a complex role in cancer. Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive sarcomas with frequent loss-of-function mutations in PRC2 that are associated with poor outcome. Here, we identify a critical role for PRC2 loss in driving MPNST metastasis. PRC2-dependent metastatic phenotypes included increased collagen-dependent invasion, upregulation of matrix-remodeling enzymes, and elevated lung metastasis in orthotopic mouse models. Furthermore, clinical sample analysis determined that PRC2 loss correlated with metastatic disease, increased fibrosis, and decreased survival in patients with MPNSTs. These results may have broad implications for PRC2 function across multiple cancers and provide a strong rationale for investigating potential therapies targeting ECM-remodeling enzymes and tumor fibrosis to improve outcomes in patients with MPNSTs.

| S-EPMC9714789 | biostudies-literature

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