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Chromatin Accessibility Analysis Reveals Distinct Functions for HDAC and EZH2 Activities in Early Regeneration

ABSTRACT: Chromatin Accessibility Analysis Reveals Distinct Functions for HDAC and EZH2 Activities in Early Regeneration

PROVIDER: PRJNA733163 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14667500_1.fastq.gz	Fastqsanger.gz
	SRR14667500_2.fastq.gz	Fastqsanger.gz
	SRR14667501_1.fastq.gz	Fastqsanger.gz
	SRR14667501_2.fastq.gz	Fastqsanger.gz
	SRR14667502_1.fastq.gz	Fastqsanger.gz

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Chromatin Accessibility Analysis Reveals Distinct Functions for HDAC and EZH2 Activities in Early Regeneration

Project description:Xenopus tropicalis tadpoles have the capability to scarlessly regenerate appendages including the limb and tail. Following injury, complex genetic processes must be activated and inactivated with high spatial and temporal resolution to result in a properly patterned appendage. Functional studies have established that histone modifying enzymes that act to close chromatin are required for regeneration, but the genomic regions sensitive to these activities are not established. Here we show that early inhibition of HDAC or Ezh2 activity results in incomplete regeneration. To identify the impact that each of these perturbations has on chromatin accessibility, we applied an assay for transposase accessible chromatin (ATAC-seq) to HDAC or Ezh2 inhibited regenerating tadpoles. We find that neither perturbation results in a global increase in chromatin accessibility, but that both inhibitors have targeted effects on chromatin accessibility and gene expression. Upon HDAC inhibition, promoter regions and regulatory regions neighboring genes associated with neuronal regeneration are precociously accessible, whereas following EZH2 inhibition we find gene bodies and regulatory regions associated with regulation of the immune response and apoptosis are preferentially accessible. Together this suggests distinct roles for EZH2 activity and HDAC activity in appendage regeneration.

2022-05-01 | GSE175662 | GEO

Genome-wide maps of H3K27me3 and H3K27ac in cells treated with HDAC inhibition, EZH2 inhibition, or combined HDAC/EZH2 inhibition

Project description:Investigation of the mechanism by which combined EZH2 and HDAC inhibition kills PC3 prostate cancer cells. Next-generation sequencing was used to identify changes in genome localization of HDAC targets (H3K27ac) and EZH2 targets (H3K27me3) upon treatment with each inhibitor alone or in combination.

2020-05-12 | GSE150336 | GEO

Genome-wide maps of H3K27me3 and H3K27ac in cells treated with HDAC inhibition, EZH2 inhibition, or combined HDAC/EZH2 inhibition

Project description:Genome-wide maps of H3K27me3 and H3K27ac in cells treated with HDAC inhibition, EZH2 inhibition, or combined HDAC/EZH2 inhibition

| PRJNA631783 | ENA

Expression data in PC3 prostate cancer cells treated with DMSO, HDAC inhibitor, EZH2 inhibitor, or combined HDAC and EZH2 inhibitors.

Project description:Expression data in PC3 prostate cancer cells treated with DMSO, HDAC inhibitor, EZH2 inhibitor, or combined HDAC and EZH2 inhibitors.

| PRJNA630152 | ENA

Delineation of EZH2 oncogenic functions in hepatocellular carcinoma

Project description:The goal of this study was to delineate the important EZH2 direct target genes that mediate the oncogenic properties of EZH2 in HCC. The EZH2 direct target genes in two HCC cell lines were identified by chromatin immunoprecipitation microarray (ChIP-chip) analysis and later confirmed by independent ChIP-PCR. The functions of the target genes were further examined. Two human HCC cell lines, Huh7 and PLC/PRF/5 (PLC5), were grown in DMEM supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-EZH2 antibody. The immunoprecipitated and input DNA were used to probe the Agilent human ChIP-chip arrays.

2011-05-31 | E-GEOD-17733 | biostudies-arrayexpress

Targeting EZH2 and HDACs in hematological cancers induces transcriptional and metabolic deregulation causing ferroptosis

Project description:The methyltransferase EZH2 functions as the enzymatic component of the PRC2 complex, which deposits methyl groups on H3K27, leading to chromatin condensation and gene repression. Recent studies have shown that EZH2 can also act as a transcriptional modulator, independently of the PRC2 complex and its methyltransferase activity. In this study, we demonstrate that EZH2 degradation is more effective in blocking cellular proliferation compared to EZH2 enzymatic inhibition. Strikingly, the combination of EZH2 degradation and HDAC inhibition exhibited potent synergy in a broad spectrum of hematological malignancies. The dual inhibition led to increased H3K27 acetylation and transcriptional deregulation, revealing that the observed synergy is driven by metabolic reprogramming. A metabolism-centered analysis showed upregulation of cholesterol biosynthesis in several hematological malignancies upon combined inhibition of EZH2 and HDACs. Interestingly, EZH2 degradation and HDAC inhibition also independently modulate distinct metabolic pathways: EZH2 degradation enhances fatty acid biosynthesis, while HDAC inhibition activates the tricarboxylic acid (TCA) cycle. The overactivation of cholesterol and fatty acid synthesis, of the TCA cycle, and histone hyperacetylation, strongly suggests induction of metabolic stress. Indeed, as a result of EZH2 degradation and HDAC inhibition, we observed an increase of reactive oxygen species (ROS), promoting lipid peroxidation and ultimately triggering ferroptotic cell death. Together, our findings highlight that co-targeting EZH2 and HDAC leads to an increase of histone acetylation and the overactivation of several metabolic pathways, leading to strong metabolic stress and induction of ferroptotic cell death.

2025-09-12 | GSE306205 | GEO

Delineation of EZH2 oncogenic functions in hepatocellular carcinoma

2011-05-31 | GSE17733 | GEO

Dissecting and Targeting Noncanonical Functions of EZH2 in Multiple Myeloma via an EZH2 Degrader [RNA-seq]

Project description:Multiple myeloma (MM) is the second most common hematological malignancy with poor prognosis. Enhancer of zeste homolog 2 (EZH2) is the enzymatic subunit of polycomb repressive complex 2 (PRC2), which catalyzes trimethylation of histone H3 lysine 27 (H3K27me3) for transcriptional repression. EZH2 have been implicated in numerous hematological malignancies, including MM. However, noncanonical functions of EZH2 in MM tumorigenesis are not well understood. Here, we uncovered a noncanonical function of EZH2 in MM malignancy. In addition to the PRC2-mediated and H3K27me3-dependent canonical function, EZH2 interacts with cMyc and co-localizes with gene activation markers, promoting MM tumorigenesis in a PRC2- and H3K27me3-independent manner. Both canonical EZH2-PRC2 and noncanonical EZH2-cMyc complexes can be effectively depleted in MM cells by MS177, an EZH2 degrader we reported previously, leading to profound activation of EZH2-PRC2-associated genes and suppression of EZH2-cMyc oncogenic nodes. The MS177-induced degradation of both canonical EZH2-PRC2 and noncanonical EZH2-cMyc complexes also reactivated immune response genes in MM cells. Phenotypically, targeting of EZH2’s both canonical and noncanonical functions by MS177 effectively suppressed the proliferation of MM cells both in vitro and in vivo. Collectively, this study uncovers a new noncanonical function of EZH2 in MM tumorigenesis and provides a novel therapeutic strategy, pharmacological degradation of EZH2, for treating EZH2-dependent MM.

2023-01-25 | GSE214668 | GEO

Dissecting and Targeting Noncanonical Functions of EZH2 in Multiple Myeloma via an EZH2 Degrader [CUT&RUN]

2023-01-25 | GSE214667 | GEO

Coordinated activities of EZH2 and EZH1 are essential for neurogenesis

Project description:Polycomb group proteins (PcG) are well known by their function in the regulation of developmental processes. PcG mediated regulation of genetic programs required for proper development are triggered by EZH2 H3K27 methyltransferase activity. EZH1 can partially substitute EZH2 activity. However, unlike EZH2, EZH1 is presence in differentiated and adult tissues suggesting additional biological functions. Here we show that EZH2 is predominantly expressed in neural stem cells being essential for neural stem cells self renewal and homeostasis. There, it controls the transcriptional state of cell cycle regulators, such as CIP1. But it is also necessary to regulate genes involved in surveillance and neuroepithelial polarity. In contrast, EZH1 expression is more abundant in differentiated cells within the spinal cord and its downregulation unables neural stem cells to differentiate. All together our data reveal a complementary but non-redundant role of EZH2 and EZH1 in neurogenesis.

2016-05-24 | GSE39450 | GEO

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