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Mutant EZH2 alters the epigenetic network and increases epigenetic heterogeneity in B cell lymphoma (CUT&Run)

ABSTRACT: Mutant EZH2 alters the epigenetic network and increases epigenetic heterogeneity in B cell lymphoma (CUT&Run)

PROVIDER: PRJNA1139185 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29931257_1.fastq.gz	Fastqsanger.gz
	SRR29931257_2.fastq.gz	Fastqsanger.gz
	SRR29931258_1.fastq.gz	Fastqsanger.gz
	SRR29931258_2.fastq.gz	Fastqsanger.gz
	SRR29931259_1.fastq.gz	Fastqsanger.gz

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Mutant EZH2 alters the epigenetic network and increases epigenetic heterogeneity in B cell lymphoma (CUT&Run)

Project description:Diffuse large B cell lymphomas and follicular lymphomas show recurrent mutations in epigenetic regulators; among these are loss-of-function mutations in KMT2D and gain-of-function mutations in EZH2. To systematically explore the effects of these mutations, alone or in combination, on the epigenetic landscape, we applied a single cell approach, based on Cytometry by Time of Flight (CyTOF), to probe a wide array of histone modifications. We show that mutant-EZH2 elicits extensive effects on the epigenome of lymphomas, beyond alterations to H3K27 methylations, and is dominant over KMT2D mutations. Utilizing the single-cell data, we present computational methods to measure epigenetic heterogeneity. We identify an unexpected characteristic of mutant-EZH2, but not KMT2D, in increasing heterogeneity, shedding light on a novel oncogenic mechanism mediated by this mutation. Finally, we present analysis to reveal potential cross talk between various modifications in the epigenetic network, validated by functional perturbations. Our work highlights novel roles for mutant-EZH2 in lymphomagenesis and establishes new concepts for measuring epigenetic heterogeneity and intra-chromatin connectivity in cancer cells

2025-01-31 | GSE272889 | GEO

Mutant EZH2 alters the epigenetic network and increases epigenetic heterogeneity in B cell lymphoma

Project description:Mutant EZH2 alters the epigenetic network and increases epigenetic heterogeneity in B cell lymphoma

| PRJNA998470 | ENA

Mutant EZH2 alters the epigenetic network and increases epigenetic heterogeneity in B cell lymphoma

2024-12-31 | GSE238258 | GEO

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation

Project description:Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. Further, we show antagonism between SNF5 and EZH2 in the regulation of stem cell-associated programs and that Snf5 loss activates those programs. Finally, using conditional mouse models, we show that inactivation of Ezh2 blocks tumor formation driven by Snf5 loss. Mouse Embryonic Fibroblasts (MEFs) conditionally inactivated for Ezh2, Snf5 and Ezh2, or from control WT MEFs were used to evaluated epigenetic antagonism between Snf5 and Ezh2 in the control of gene expression programs. Snf5-deficient lymphoma samples and control CD8+ WT T-cells were used to evaluate genetic programs misregulated by Snf5 inactivation during tumorigenesis. RNA was isolated from each of these samples and used for gene expression profiling on Affymetrix arrays.

2010-10-19 | E-GEOD-23656 | biostudies-arrayexpress

CUT & RUN H3K27me3 of Human Naïve and Primed Pluripotent Stem Cells with and without EZH2 inhibition.

Project description:CUT & RUN H3K27me3 of Human Naïve and Primed Pluripotent Stem Cells with and without EZH2 inhibition.

2022-03-23 | GSE183735 | GEO

CUT&RUN Sequencing of EZH2 binding sites in HEK293T cells expressing a Dual-specificity Aptamer that specifically increases O-GlcNAcylation on beta-catenin

Project description:O-GlcNAc is a dynamic post-translational modification on thousands of intracellular proteins, it regulates protein functions and is involved in many metabolic diseases. Using a dual-specificity aptamer, we targeted the O-GlcNAc transferase (OGT) to endogenous β-catenin and specifically increased O-GlcNAcylation of β-catenin. We found that O-GlcNAc on β-catenin promoted its interaction with EZH2 regardless of the Wnt signaling status. To study how this interaction regulates the distribution of EZH2 on the genome, we performed Cleavage Under Targets and Release Using Nuclease (CUT&RUN) on HEK293T cells expressing individual (Ctrl.) or dual-specificity aptamers. Under Wnt - and Wnt + conditions, the dual-specificity aptamer increased the binding of EZH2 on 923 and 3473 genomic sites, respectively. These two sets of differential binding sites showed little overlap.

2022-11-30 | GSE190172 | GEO

Epigenetic Maintenance of Stemness and Malignancy in Peripheral Neuroectodermal Tumors by EZH2

Project description:Chromatin modifications are increasingly recognized as a key mechanism in cancer. The histone methyl-transferase Enhancer of Zeste, Drosophila, Homolog 2 (EZH2) is the enzymatic subunit of the polycomb PRC2 complex and methylates histone H3K27, thereby, mediating gene silencing. Down-regulation of EZH2 by RNA interference in ET suppressed oncogenic transformation, tumor development and metastasis in a respective mouse model. Further microarray analysis of EZH2 knock down, or functionally linked HDAC-inhibitor treatment revealed an undifferentiated reversible phenotype in ET maintained by EZH2. EZH2 suppression resulted in a generalized loss of H3K27me3 as well as an increase in H3 acetylation levels. In addition, ChIP-Chip assays for H3K27me3 identified genes that had specifically lost H3K27me3 upon EZH2 silencing. These findings suggested that stemness features are preserved via epigenetic mechanisms. Taken together, the genetic EWS-Fli1 translocation is intimately linked to global and gene specific epigenetic alterations in ET biology. EZH2 mediates neuroectodermal and endothelial embryonal tumor stem cell growth and metastasic spread induced by a translocation derived chimeric transcription factor. Keywords: PNET, Ewing Tumor Epigenetic regulation A673 transiently transfected with siRNA-EZH2 and siRNA-scrambled were harvested and Chromatin-IPs of H3K27me3 or H3 followed by microarray hybridisation were carried out. For detailed procedures see Burdach et al. Epigenetic Maintenance of Stemness and Malignancy in Peripheral Neuroectodermal Tumors by EZH2.

2010-05-18 | E-GEOD-15890 | biostudies-arrayexpress

Epigenetic profiling of prostate adenocarcinoma and neuroendocrine prostate cancer models to understand EZH2 activity. [Cut & Run]

Project description:Epigenetic profiling of prostate adenocarcinoma and neuroendocrine prostate cancer models to understand EZH2 activity. [Cut & Run]

| PRJNA1078705 | ENA

Cut and Run ChIP-seq of SUZ12 and EZH2 in cadmium resistant breast cancer MDA-231 cells

Project description:In this study we compared genome wide SUZ12 and EZH2 Cut&RUN CHIP-seq of cadmium resistant MDA-231 breast cancer cells vs untreated controls.

2021-07-13 | GSE179823 | GEO

Targeting EZH2 increases the vulnerability of triple-negative breast cancer

Project description:Targeting EZH2 increases the vulnerability of triple-negative breast cancer

| PRJNA445854 | ENA