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Transcriptome Analysis of PRC2 isogenic human MPNST cells with or without DNA demethylating therapy (RNA-Seq)

ABSTRACT: Goals of this study were to determine the effect of PRC2 loss or DNA demethylating therapy either alone or in combination on the Transcriptome

ORGANISM(S): Homo sapiens

PROVIDER: GSE179585 | GEO | 2022/11/17

REPOSITORIES: GEO

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CpG DNA methylation analysis of PRC2 isogenic human MPNST cells with or without DNA demethylating therapy (Methyl-Seq)

Project description:Goals of this study were to determine the effect of PRC2 loss or DNA demethylating therapy either alone or in combination on CpG DNA methylation genome wide

2022-11-17 | GSE179586 | GEO

Genome wide maps of histone modifications in PRC2 isogenic human MPNST cells with or without DNA demethylating therapy (ChIP-Seq)

Project description:Goals of this study were to determine the effect of PRC2 loss or DNA demethylating therapy (GSK862 and DAC) either alone or in combination on histone modifications.

2022-08-17 | GSE179582 | GEO

Analysis of PRC2 isogenic human MPNST cells with or without DNA demethylating therapy

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

2022-08-17 | GSE179587 | GEO

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.

2022-08-17 | GSE179699 | GEO

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.

2022-08-17 | GSE206527 | GEO

PRC2

Project description:PRC2

| PRJNA761389 | ENA

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.

2024-03-01 | GSE226980 | GEO

H3K27 Methyltransferase PRC2 Represses Wnt Genes to Facilitate Adipogenesis

Project description:The Wnt/b-catenin signaling inhibits adipogenesis. Genome-wide profiling studies have revealed the enrichment of histone H3K27 methyltransferase PRC2 on Wnt genes. However, the functional significance of such a direct link between the two types of developmental regulators in mammalian cells, and the role of PRC2 in adipogenesis, remain unclear. Here we show PRC2 and its H3K27 methyltransferase activity are required for adipogenesis. PRC2 directly represses Wnt1, 6, 10a and 10b genes in preadipocytes and during adipogenesis. Deletion of the enzymatic Ezh2 subunit of PRC2 eliminates H3K27me3 on Wnt promoters and de-represses Wnt expression, which leads to activation of Wnt/b-catenin signaling and inhibition of adipogenesis. Ectopic expression of the wild type Ezh2, but not the enzymatically inactive F667I mutant, prevents the loss of H3K27me3 and the defects in adipogenesis in Ezh2-/- preadipocytes. The adipogenesis defects in Ezh2-/- cells can be rescued by expression of adipogenic transcription factors PPARa, C/EBPb, or inhibitors of Wnt/b-catenin signaling. Interestingly, Ezh2-/- cells show marked increase of H3K27 acetylation globally as well as on Wnt promoters. These results indicate that H3K27 methyltransferase PRC2 directly represses Wnt genes to facilitate adipogenesis, and suggest that acetylation and trimethylation on H3K27 play opposing roles in regulating Wnt expression. To identify additional PRC2-regulated genes in preadipocytes, we performed microarray analysis in Ezh2flox/flox preadipocytes infected with retroviruses expressing Cre or vector alone.

2010-03-19 | E-GEOD-20054 | biostudies-arrayexpress

RNA-seq dataset for MPNST cell lines

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

2021-06-28 | GSE141437 | GEO

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