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

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

PROVIDER: PRJNA744564 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15066751_1.fastq.gz	Fastqsanger.gz
	SRR15066751_2.fastq.gz	Fastqsanger.gz
	SRR15066752_1.fastq.gz	Fastqsanger.gz
	SRR15066752_2.fastq.gz	Fastqsanger.gz
	SRR15066753_1.fastq.gz	Fastqsanger.gz

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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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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.

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

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

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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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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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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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UBIQUITIN LIGASE STUB1 DESTABILIZES IFNγ-RECEPTOR COMPLEX TO SUPPRESS TUMOR IFNγ SIGNALING

Project description:The cytokine IFNγ differentially impacts on tumors upon immune checkpoint blockade (ICB). Despite our understanding of downstream signaling events, less is known about 36 regulation of its receptor (IFNγ-R1). With an unbiased genome-wide CRISPR/Cas9 screen for critical regulators of IFNγ-R1 cell surface abundance, we identified STUB1 as an E3 ubiquitin ligase for IFNγ-R1 in complex with its signal-relaying kinase JAK1. STUB1 mediates ubiquitination-dependent proteasomal degradation of IFNγ-R1/JAK1 complex through IFNγ-R1K285 and JAK1K249. Conversely, STUB1 inactivation amplifies IFNγ signaling, sensitizing tumor cells to cytotoxic T cells in vitro. This was corroborated by an anticorrelation between STUB1 expression and IFNγ response in ICB-treated patients. Consistent with the context-dependent effects of IFNγ in vivo, anti-PD-1 response was increased in heterogenous tumors comprising both wildtype and STUB1-deficient cells but not full STUB1 knockout tumors. These results uncover STUB1 as a critical regulator of IFNγ-R1, and highlight the context-dependency of STUB1-regulated IFNγ signaling for ICB outcome.

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Project description:Imprinted X-inactivation is a paradigm of transgenerational epigenetic inheritance in mammals and silences genes exclusively on the paternally-inherited X-chromosome. Here, we test the hypothesis that oocyte-derived maternal Polycomb repressive complex 2 (PRC2) protein EED orchestrates the selective inactivation of the paternal-X in mouse embryos. In maternal Eed null (Eedm-/-) but not zygotic Eed null female and male embryos, the maternal X-chromosome ectopically induced Xist lncRNA, which silences X-linked genes. Subsequently, Xist was silenced from one of the two X-chromosomes in females and from the sole maternal-X in males. As a result, later-stage female Eedm-/- embryos displayed random X-inactivation. The kinetics of Xist RNA induction in Eedm-/- embryos resemble that of early human embryos, which lack oocyte-derived PRC2 and only undergo random X-inactivation. Thus, expression of PRC2 genes in the oocyte and transmission of the gene products to the embryo may dictate the occurrence of imprinted X-inactivation in mammals.

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