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Methylation-dependent and -independent roles of EZH2 coordinately contribute to CDCA8 activation in prostate cancer

ABSTRACT: Methylation-dependent and -independent roles of EZH2 coordinately contribute to CDCA8 activation in prostate cancer

PROVIDER: PRJNA766037 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16048106.fastq.gz	Fastqsanger.gz
	SRR16048107.fastq.gz	Fastqsanger.gz
	SRR16048108.fastq.gz	Fastqsanger.gz
	SRR16048109.fastq.gz	Fastqsanger.gz
	SRR16048110.fastq.gz	Fastqsanger.gz

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Methylation-dependent and -independent roles of EZH2 coordinately contribute to CDCA8 activation in prostate cancer

Project description:Cell division cycle associated 8 (CDCA8) is a component of chromosomal passenger complex (CPC) that participates in mitotic regulation. Although cancer-related CDCA8 hyperactivation has been widely observed, its molecular mechanism remains elusive. Here, we report that CDCA8 overexpression maintains tumorigenicity and is associated with poor clinical outcome in patients with prostate cancer (PCa). Notably, enhancer of zeste homologue 2 (EZH2) is identified to be responsible for CDCA8 activation in PCa. Genome-wide assays revealed that EZH2-induced H3K27 trimethylation represses let-7b expression and thus protects the let-7b-targeting CDCA8 transcripts. More importantly, EZH2 facilitates the self-activation of E2F1 by recruiting E2F1 to its own promoter region in a methylation-independent manner. The high level of E2F1 further promotes transcription of CDCA8 along with the other CPC subunits. Taken together, our study suggests that EZH2-mediated cell cycle regulation in PCa relies on both its methyltransferase and non-methyltransferase activities.

2021-09-30 | GSE184740 | GEO

Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator

Project description:Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator

| PRJNA421353 | ENA

Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [microarray]

Project description:Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [microarray]

| PRJNA421357 | ENA

Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [microarray]

Project description:EZH2 induces active transcription of the AR gene, thereby increasing AR level and promoting AR signaling. Importantly, EZH2-mediated activation of AR requires EZH2 protein occupancy at the AR gene promoter, but is independent of PRC2 as well as its histone methyltransferase activity

2018-12-01 | GSE107779 | GEO

Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [RNA-seq]

Project description:Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [RNA-seq]

| PRJNA421358 | ENA

Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [ChIP-seq]

Project description:Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [ChIP-seq]

| PRJNA421359 | ENA

Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [RNA-seq]

2018-12-01 | GSE107781 | GEO

Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator [ChIP-seq]

2018-12-01 | GSE107780 | GEO

Dual and separable roles for Ezh2 in neurogenic astroglia

Project description:The epigenetic mechanisms that enable specialized astrocytes to retain neurogenic competence throughout adult life are still poorly understood. Here we show that astrocytes that serve as neural stem cells (NSCs) in the adult mouse subventricular zone (SVZ) express the histone methyltransferase EZH2. This Polycomb repressive factor is required for neurogenesis independent of its role in SVZ NSC proliferation, as Ink4a/Arf-deficiency in Ezh2-deleted SVZ NSCs rescues cell proliferation, but neurogenesis remains defective. Olig2 is a direct target of EZH2, and repression of this bHLH transcription factor is critical for neuronal differentiation. Furthermore, Ezh2 prevents the inappropriate activation of genes that specify non-SVZ neuronal subtypes. In the human brain, SVZ cells including local astroglia also express EZH2, correlating with postnatal neurogenesis. Thus, EZH2 is an epigenetic regulator that distinguishes neurogenic SVZ astrocytes, orchestrating distinct and separable aspects of adult stem cell biology, which has important implications for regenerative medicine and oncogenesis. Examination of histone modifications (H3K27me3 and H3K4me3) in subventricular zone neural stem cells

2014-05-02 | E-GEOD-56394 | biostudies-arrayexpress

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

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