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Homo sapiens

ABSTRACT: Identifying ASCL1-mediated chromatin changes in primary GBM stem cell cultures [ATAC-seq]

PROVIDER: PRJNA354999 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5057780.fastq.gz	Fastqsanger.gz
	SRR5057781.fastq.gz	Fastqsanger.gz
	SRR5057782.fastq.gz	Fastqsanger.gz
	SRR5057783.fastq.gz	Fastqsanger.gz

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Identifying ASCL1-mediated chromatin changes in primary GBM stem cell cultures [ATAC-seq]

Project description:ASCL1 mediates neuronal differentiation of GBM stem cell (GSC) cultures. We sought to identify chromatin changes upon induced ASCL1 expression in primary human GSC cultures. In this dataset, we include ATAC-seq data obtained from GSC cultures harbouring a CRISPR-deletion of ASCL1. We assessed differential ASCL1 binding between control and GSC cultures induced to overexpress ASCL1 after 14 days of doxycycline treatment.

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Identifying ASCL1 target genes in primary GBM stem cell cultures [ChIP-seq]

Project description:ASCL1 mediates neuronal differentiation of GBM stem cell (GSC) cultures. We sought to identify genomic targets of ASCL1 in primary human GSC cultures. In this dataset, we include ChIP-seq data obtained from GSC cultures harbouring a CRISPR-deletion of ASCL1. We assessed differential ASCL1 binding between control and GSC cultures induced to overexpress ASCL1 after 18 hours of doxycycline treatment.

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Project description:Primary glioblastoma (GBM) cultures vary with respect to differentiation competency. We sought to identify putative transcription factors necessary for the differentiation of GBM cultures. In this dataset, we include expression data obtained from 2 human-fetal neural stem cell (HF-NS) cultures and 2 GBM stem cell (GSC) cultures. We assessed changes in gene expression from 3 timepoints during an in vitro differentiation protocol.

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Project description:Glioblastoma (GBM) is thought to be driven by a sub-population of cancer stem cells (CSCs) that self-renew and recapitulate tumor heterogeneity, yet remain poorly understood. Here we present a comparative epigenomic analysis of GBM CSCs that reveals widespread activation of genes normally held in check by Polycomb repressors. These activated targets include a large set of developmental transcription factors (TFs) whose coordinated activation is unique to the CSCs. We demonstrate that a critical factor in the set, ASCL1, activates Wnt signaling by repressing the negative regulator DKK1. We show that ASCL1 is essential for maintenance and in vivo tumorigenicity of GBM CSCs. Genomewide binding profiles for ASCL1 and the Wnt effector LEF1 provide mechanistic insight and suggest widespread interactions between the TF module and the signaling pathway. Our findings demonstrate regulatory connections between ASCL1, Wnt signaling and collaborating TFs that are essential for the maintenance and tumorigenicity of GBM CSCs. Histone modification profiling for multiple marks by ChIP-Seq in untreated glioblastoma cancer stem cells, glioblastoma non-stem cells and neural stem cells

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