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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179582 | GEO | 2022/08/17

REPOSITORIES: GEO

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

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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

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

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

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DNA methylation analysis of cloned HCT116 cells treated with a DNA demethylating drug.

Project description:Epigenetic reprogramming using demethylating drugs is a promising approach for cancer therapy, but its efficacy is highly dependent on the dosing regimen. Low-dose treatment for a prolonged period shows a high therapeutic efficacy, despite its small demethylating effect. Here, we aimed to reveal the mechanisms of how such low-dose treatment shows high efficacy by focusing on epigenetic reprograming at the single-cell level. Single-cell RNA-sequencing of HCT116 cells treated with decitabine (DAC) revealed that up-regulated genes were highly variable at the single-cell level. To analyze functional consequences at the single-cell level, DAC-treated HCT116 cells were cloned. While only partial reduction of methylation levels was observed in bulk cells, complete demethylation of specific cancer-related genes was observed, depending upon clones. For example, p16 was completely demethylated in the H3-32 clone out of 9 clones, and this clone showed slower proliferation than other clones without demethylation. In addition, in this clone, the fraction of cells with tetraploid became much larger, indicating that cellular senescence was induced. These results showed that epigenetic reprogramming of specific cancer-related pathways at the single-cell level is likely to underlie the high efficacy of low-dose DNA demethylating therapy.

2020-10-02 | GSE149255 | 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.

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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.

2022-08-17 | GSE206527 | GEO

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Project description:PRC2

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The impact of decitabine treatment in MDS-induced Tet2KD/KDEzh2Δ/Δ LSK HSPCs

Project description:To evaluate the impact of DNA demethylating agents on our mouse MDS model, we chose 5-aza-2’-deoxycytidine, decitabine (DAC), one of the DNA demethylating agents, which is incorporated into DNA but not RNA and has 10-fold more potency in DNA demethylation than 5-azacitidine. We transplanted Tet2KD/KDEzh2Δ/Δ MDS cells into lethally irradiated secondary recipients and treated them with DAC (low dose DAC at 0.25mg/kg, 3 times a week, intraperitoneal injection), then purified LSK HSPCs and evaluated the expression profiles.

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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.

2022-08-17 | GSE179699 | GEO

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