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An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27m3 through the genome

ABSTRACT: An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27m3 through the genome

OTHER RELATED OMICS DATASETS IN: GSE79036

PROVIDER: PRJNA314766 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3213590_1.fastq.gz	Fastqsanger.gz
	SRR3213590_2.fastq.gz	Fastqsanger.gz
	SRR3213620.fastq.gz	Fastqsanger.gz
	SRR3213630.fastq.gz	Fastqsanger.gz
	SRR3213591_1.fastq.gz	Fastqsanger.gz

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An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27m3 through the genome [RNA-seq]

Project description:B-cell lymphoma and melanoma harbor recurrent mutations in the gene encoding the EZH2 histone methyltransferase, but the carcinogenic role of these mutations is unclear. Here we describe a mouse model in which the most common somatic EZH2 gain-of-function mutation (Y646F in human, Y641F in the mouse) can be conditionally expressed. Expression of Ezh2Y641F in mouse B-cells or melanocytes caused high-penetrance lymphoma or melanoma, respectively. Bcl2 overexpression or p53 loss, but not c-Myc overexpression, further accelerated lymphoma progression, and expression of mutant B-Raf but not mutant N-Ras further accelerated melanoma progression. Although expression of Ezh2Y641F increased abundance of global H3K27 trimethylation (H3K27me3), it also caused a widespread redistribution of this repressive mark, including a loss of H3K27me3 associated with increased transcription at many loci. These results suggest that Ezh2Y641F induces lymphoma and melanoma through a vast reorganization of chromatin structure inducing both repression and activation of polycomb-regulated loci. B cells: 4 WT vs 4 Y641F samples, Melanoma: WT (480, 855) vs Y641F (480D, 855D) isogenic cell lines differing only for the presence of WT vs Y641F Ezh2.

2016-05-13 | E-GEOD-79035 | biostudies-arrayexpress

An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27m3 through the genome [RNA-seq]

2016-05-13 | GSE79035 | GEO

Mus musculus

Project description:An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27m3 through the genome [RNA-seq]

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An oncogenic Ezh2 mutation cooperates with particular genetic alterations to induce tumors in mice and redistributes H3K27m3 through the genome

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

2016-05-02 | GSE79036 | GEO

Truncated BRPF1 cooperates with Smoothened to induce adult Shh medulloblastoma

Project description:Truncated BRPF1 cooperates with Smoothened to induce adult Shh medulloblastoma

| PRJNA525143 | ENA

Oncogenic Lmo3 cooperates with Hen2 to induce hydrocephalus in mice.

Project description:We previously reported that LMO3 and HEN2 act as oncogenes in neuroblastoma development through up-regulating MASH1 transcription by interfering with HES1. To confirm these results in vivo, we generated transgenic mice of these genes. Lmo3 or Hen2 was expressed under the control of Wnt1 promoter, which is expressed in the central nervous system and neural crest of the sympathoadrenal lineage from which neuroblastoma develops. Heterozygous Lmo3 and Hen2 transgenic mice (Tg (Lmo3) and Tg (Hen2)) developed hydrocephalus at higher frequency than for the wild type mice, and all heterozygous double-transgenic mice (Tg (Lmo3; Hen2)) developed hydrocephalus. Therefore, Lmo3 and Hen2 may be involved in and have synergistic effects on hydrocephalus development. Although aqueduct stenosis occurred in all genotypes, it was mild in Tg (Lmo3; Hen2) mice. Furthermore, hydrocephalus was detected at E18.5 in Tg (Lmo3; Hen2). These results suggest that the causes of hydrocephalus are not only aqueduct stenosis but also disorder of neocortical development. A similar phenotype was reported in Robo1/2(-/-) mice, in which Hes1 expression level was decreased in ventricular zone progenitors. Thus, it is suggested that the expression levels of Lmo3 and/or Hen2 could determine the fate of stem cells by inhibiting Hes1 function during nervous system development and might be a trigger of aberrant neurogenesis in vivo.

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Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

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

Cre-recombinase expression cooperates with FLT3ITD/ITD to induce acute myeloid leukemia

Project description:Cre-recombinase expression cooperates with FLT3ITD/ITD to induce acute myeloid leukemia

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Inhibition of the epigenetic regulator Ezh2 redistributes bivalent domains within transcriptional regulators associated with Wnt and Hedgehog pathways

Project description:Inhibition of the epigenetic regulator Ezh2 redistributes bivalent domains within transcriptional regulators associated with Wnt and Hedgehog pathways

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