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Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma [RNA-Seq]

ABSTRACT: Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma [RNA-Seq]

PROVIDER: PRJNA1006404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25670942_1.fastq.gz	Fastqsanger.gz
	SRR25670942_2.fastq.gz	Fastqsanger.gz
	SRR25670943_1.fastq.gz	Fastqsanger.gz
	SRR25670943_2.fastq.gz	Fastqsanger.gz
	SRR25670944_1.fastq.gz	Fastqsanger.gz

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Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma

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Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma [CUT&RUN]

Project description:Osteosarcomas (OS) are aggressive bone tumors characterized by extensive structural variation, and rare recurrent oncogenic driver mutations. Here, we identify ectopic expression of the oncohistone-mimic EZHIP in more than 20% of patients, in two independent OS cohorts. Through gain- and loss-of-function experiments, we provide evidence that EZHIP expression is oncogenic, increasing the aggressive features of OS in vitro and in vivo. EZHIP-mediated epigenetic rewiring promotes reactivation of developmental transcriptional programs and stalled differentiation of mesenchymal progenitors, which are skewed towards smooth muscle commitment at the expense of other lineages. Our findings of EZHIP expression as a prevalent driver in OS provide new insights into pathogenic pathways and therapeutic alternatives for this debilitating cancer.

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H3 K27M and EZHIP impede H3K27-methylation spreading by inhibing allosterically stimulated PRC2 [EZHIP]

Project description:In this study, we report that EZHIP and H3 K27M preferentially interact with an allosterically activated form of PRC2 in vivo. The formation of H3 K27M- and EZHIP-PRC2 complexes occurs at CpG islands containing H3K27me3 and impedes PRC2 and H3K27me3 spreading. Moreover, we find that H3 K27M inhibits PRC2 in trans and can reduce H3K27me3 levels independent of chromatin incorporation. While EZHIP is not found outside of placental mammals, we find that expression of human EZHIP reduces H3K27me3 in Drosophila melanogaster through a conserved molecular mechanism.

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Histone H3 wild-type DIPG/DMG overexpressing EZHIP extend the spectrum diffuse midline gliomas with PRC2 inhibition beyond H3-K27M mutation

Project description:Characterisation of a new subgroup of DMG lacking H3-K27M mutation that is defined by H3K27me3 loss and EZHIP overexpression that can be detected by IHC. These tumors are distinct from EZHIP-positive posterior fossa ependymomas and are associated with a dismal prognosis. We propose that these EZHIP/H3-WT tumors need to be considered similar to canonical DIPG/DMG, thus extending the spectrum of DMG with PRC2 inhibition beyond H3-K27M mutation

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Identification of novel candidate oncogenes in chromosomal region 17p11.2-p12 in human osteosarcoma

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