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Integrated Analysis of Genes Encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

ABSTRACT: Integrated Analysis of Genes Encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

PROVIDER: PRJNA793704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17406682_1.fastq.gz	Fastqsanger.gz
	SRR17406682_2.fastq.gz	Fastqsanger.gz
	SRR17406683_1.fastq.gz	Fastqsanger.gz
	SRR17406683_2.fastq.gz	Fastqsanger.gz
	SRR17406684_1.fastq.gz	Fastqsanger.gz

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Integrated Genomic Analysis of Genes encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

Project description:Integrated Genomic Analysis of Genes encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

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Integrated Analysis of Genes Encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

Project description:We experimentally demonstrated that CHD7 promotes the growth of colorectal cancer cells in vitro and in vivo. Mechanistically, RNA-seq and ATAC-seq approaches together with ChIP assays indicated that CHD7 can bind to the promoters of target genes to maintain chromatin accessibility and facilitate transcription. We found that CHD7 knockdown downregulates AK4 expression and activates AMPK phosphorylation, thereby promoting the phosphorylation and stability of p53 and leading to the inhibition of the colorectal cancer growth. Our genomic analyses of ATPCRs across large-scale cancer specimens identified potential therapeutic targets and our experimental studies revealed a novel CHD7-AK4-AMPK-p53 axis that plays an oncogenic role in colorectal cancer.

2022-01-04 | GSE192905 | GEO

Integrated Genomic Analysis of Genes encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

Project description:To decipher how CHD7 knockdown affects the growth of colorectal cancer cells, we undertook an unbiased genomic approach to define the transcriptional program controlled by CHD7 in RKO cells.

2022-01-01 | GSE192725 | GEO

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [ChIP-seq]

Project description:Mutations in CHD7, encoding ATP-dependent chromodomain-helicase-DNA-binding protein 7, in CHARGE syndrome leads to multiple congenital anomalies including growth retardation, craniofacial malformations and neurological dysfunction. Currently, mechanisms underlying the CNS phenotypes remain poorly understood. Here, we show that Chd7 is a direct transcriptional target of oligodendrogenesis-promoting factors Olig2 and Brg1 and required for proper timing of CNS myelination and remyelination. Genome-occupancy analyses coupled with transcriptome profiling reveal that Chd7 cooperates with Sox10 to target the enhancers of key myelinogenic genes, and identify novel Chd7 target. Examination of Chd7 and Sox10 genomewide occupancy in differentiating oligodendrocytes

2016-02-29 | E-GEOD-72725 | biostudies-arrayexpress

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [RNA-seq]

Project description:Mutations in CHD7, encoding ATP-dependent chromodomain-helicase-DNA-binding protein 7, in CHARGE syndrome leads to multiple congenital anomalies including growth retardation, craniofacial malformations and neurological dysfunction. Currently, mechanisms underlying the CNS phenotypes remain poorly understood. Here, we show that Chd7 is a direct transcriptional target of oligodendrogenesis-promoting factors Olig2 and Brg1 and required for proper timing of CNS myelination and remyelination. Genome-occupancy analyses coupled with transcriptome profiling reveal that Chd7 cooperates with Sox10 to target the enhancers of key myelinogenic genes, and identify novel Chd7 target. 4 RNA-Seq samples from P8 spinal cords of Ctrl and Chd7 cKO mice (duplicatess, Ctrl and cKO)

2016-02-29 | E-GEOD-72726 | biostudies-arrayexpress

Expression profiles in Chd7 knockdown oligodendrocyte precursor cells

Project description:Oligodendrocytes are generated from oligodendrocyte precursor cells (OPCs). Chd7 is ATP-dependent chromatin-remodeling enzyme. We performed microarray analysis to examine changes in gene expression between control and Chd7 knockdown OPCs. Results provide insight into the function of Chd7 in oligodendrocyte development.

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CHD7 controls cerebellar development via Reelin

Project description:Mutation of the gene encoding the ATP-dependent chromatin remodeler CHD7 causes CHARGE syndrome. The mechanisms underlying the neurodevelopmental deficits associated with the syndrome, which include cerebellar hypoplasia, developmental delay, coordination problems and autistic features, are not known. CHD7 is expressed in neural stem and progenitor cells, but its role in neurogenesis during brain development remains unknown. Here we show that deletion of Chd7 from cerebellar granule cell precursors (GCps) in the mouse results in reduced GCp proliferation, cerebellar hypoplasia, developmental delay and motor deficits. Genome-wide expression profiling revealed downregulated Reln gene expression in Chd7-deficient GCps. Recessive RELN mutations is associated with severe cerebellar hypoplasia in humans. We provide molecular and genetic evidence that reduced Reln expression contributes substantially to the GCp proliferative defect and cerebellar hypoplasia in GCp-specific Chd7 mouse mutants. Finally, we show that CHD7 is necessary for the maintenance of an open, accessible chromatin state at the Reln locus. Taken together, this study shows that Reln gene expression is regulated by chromatin remodeling, identifies CHD7 as a previously unrecognized upstream regulator of Reln and provides the first evidence that a mammalian CHD protein controls brain development by modulating chromatin accessibility in neuronal progenitors in vivo.

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Genome-wide distribution and function of ATP-dependent chromatin remodelers in embryonic stem cells

Project description:This study describes the distribution and functional analysis of ATP-dependent chromatin remodelers in mouse 46C ES cells. The remodelers for which ChIP-Seq profiles were generated are Brg1, Chd1, Chd2, Chd4, Chd6, Chd8, Chd9 and Ep400. We first generated ES cell lines expressing individual remodelers fused to an affinity tag at the C-terminus, from their endogenous loci. Remodelers were then formaldehyde-crosslinked to chromatin in vivo, MNase digested to release individual nucleosomes, then immunoprecipitated sequentially with two distinct antibodies against the tag. DNA fragments immunoprecipitated with each factor were then identified by high throughput sequencing. Control experiments were realized by applying the same protocol to untagged ES cells. Pol II distribution was examined by ChIP-exo in ES cells depleted of either Ep400, Brg1 and Chd4. Chromatin access was studied by ATAC-seq in remodeler-depleted cells. Finally, nucleosomal occupancy was explored by MNase-seq.

2016-01-26 | GSE64825 | GEO

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [RNA-seq]

2016-02-29 | GSE72726 | GEO

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [ChIP-seq]

2016-02-29 | GSE72725 | GEO