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Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies

ABSTRACT: Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies

PROVIDER: PRJNA771531 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16352126_1.fastq.gz	Fastqsanger.gz
	SRR16352126_2.fastq.gz	Fastqsanger.gz
	SRR16352127_1.fastq.gz	Fastqsanger.gz
	SRR16352127_2.fastq.gz	Fastqsanger.gz
	SRR16352128_1.fastq.gz	Fastqsanger.gz

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Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies [ChIP-Seq]

Project description:Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies [ChIP-Seq]

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Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies [RNA-Seq]

Project description:Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies [RNA-Seq]

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Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies [RNA-Seq]

Project description:Glioblastomas are universally fatal cancers that contain self-renewing glioblastoma stem cells (GSCs) that initiate tumors. Traditional anti-cancer drug discovery based on in vitro cultures tends to identify targets with poor therapeutic index and fails to accurately model the effects of the tumor microenvironment. Here, leveraging in vivo genetic screening, we identified the H3K4me3 regulator DPY30 as an in vivo-specific glioblastoma dependency. Based on the hypothesis that in vivo epigenetic regulation may define critical GSC dependencies, we interrogated active chromatin landscapes of GSCs derived from intracranial xenografts and cell culture through Histone H3 lysine 4 trimethylation (H3K4me3) chromatin immunoprecipitation and transcriptome analysis. Intracranial-specific genes marked by H3K4me3 included FOS, NFkB, and phosphodiesterase family members. In intracranial tumors, DPY30 regulated angiogenesis and hypoxia pathways in an H3K4me3-dependent manner, but was dispensable in cultured GSCs. PDE4B was a key downstream effector of DPY30; the PDE4 inhibitor, rolipram, preferentially targeted DPY30-expressing cells and impaired in vivo glioblastoma growth without affecting cultured tumor cells. Collectively, DPY30 selectively regulates H3K4me3 modification on genes critical to support angiogenesis and tumor growth in vivo, laying the foundation for the DPY30-PDE4B axis as a specific and novel therapeutic target in glioblastoma with a broad therapeutic index.

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Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies [ChIP-Seq]

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Glioblastoma Stem Cells Reprogram Chromatin In Vivo To Generate Selective Therapeutic Dependencies

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

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Reprogram glioblastoma (GBM) human cell line into DC

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Project description:Identifying the spectrum of genes required for cancer cell survival can reveal essential cancer circuitry and therapeutic targets, but such a map remains incomplete for many cancer types. We apply genome-scale CRISPR-Cas9 loss-of-function screens to map the landscape of selectively essential genes in chordoma, a bone cancer with few validated targets. This approach confirms a known chordoma dependency, TBXT (T; brachyury), and identifies a range of additional dependencies, including PTPN11, ADAR, PRKRA, LUC7L2, SRRM2, SLC2A1, SLC7A5, FANCM, and THAP1. CDK6, SOX9, and EGFR, genes previously implicated in chordoma biology, are also recovered. We find genomic and transcriptomic features that predict specific dependencies, including interferon-stimulated gene expression, which correlates with ADAR dependence and is elevated in chordoma. Validating the therapeutic relevance of dependencies, small-molecule inhibitors of SHP2, encoded by PTPN11, have potent preclinical efficacy against chordoma. Our results generate an emerging map of chordoma dependencies to enable biological and therapeutic hypotheses.

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