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Genome-wide occupancy of ZRF1 and BRD4 in neuroblastoma cells.

ABSTRACT: Genome-wide occupancy of ZRF1 and BRD4 in neuroblastoma cells.

PROVIDER: PRJNA756174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15524794_1.fastq.gz	Fastqsanger.gz
	SRR15524794_2.fastq.gz	Fastqsanger.gz
	SRR15524795_1.fastq.gz	Fastqsanger.gz
	SRR15524795_2.fastq.gz	Fastqsanger.gz
	SRR15524796_1.fastq.gz	Fastqsanger.gz

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Genome-wide occupancy of ZRF1 and BRD4 in neuroblastoma cells.

Project description:Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through integrated proteomics and validating studies, we discovered that ZRF1 and BRD4 form a complex with p113, a novel protein derived from CUX1 circular RNA. To investigate the mechanisms underlying the oncogenic functions of ZRF1 and BRD4, we employed the Illumina Novaseq 6000 as a discovery platform to analyze the genome-wide occupancy of ZRF1 and BRD4 on target genes in human SH-SY5Y cells, while the results were further analyzed with p113-regulated target genes. The results showed that 46 target genes were regulated by transcriptional trimer complex p113/ZRF1/BRD4, especially those involved in metabolic pathway or complex I biogenesis, including ALDH3A1, NDUFA1, and NDUFAF5. Furthermore, we validated the ChIP-seq results by real-time PCR with high identity. Overall, our results provided fundamental information about the genomic enrichment of ZRF1 and BRD4 in human NB cells, and these findings will help us understand the pathogenesis of NB.

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Genome-wide occupancy of CNBP and SMARCC2 in neuroblastoma cells.

Project description:Genome-wide occupancy of CNBP and SMARCC2 in neuroblastoma cells.

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Brd4, H3K27Ac, and H3K36me3 binding profiles with or without Dinaciclib in human neuroblastoma CLB-GA cells

Project description:Promoter rearrangement of the telomerase reverse transcriptase (TERT) gene juxtaposes the coding sequence to strong enhancer elements, leading to TERT overexpression and poor prognosis. TERT associated oncogenic signaling in neuroblastoma remains unclear. Gene set enrichment analysis of RNA-seq data from 498 neuroblastoma patients revealed a coordinated activation of oncogenic signaling pathways and differentially overexpressed gene signature in a subgroup of MycN non-amplified neuroblastomas with TERT overexpression. ChIP-seq analysis of human neuroblastoma cell line CLB-GA harboring TERT rearrangement uncovered genome-wide chromatin co-occupancy of Brd4 and H3K27Ac and robust enrichment of H3K36me3 in TERT and multiple TERT-associated genes. We demonstrated a critical regulatory role of Brd4 and cyclin-dependent kinases in the expression and chromatin activation. Inhibition of both with AZD5153 and dinaciclib proved most effective in tumor growth suppression of neuroblastoma cell lines, primary cells, and xenograft. Our study provides a therapeutic strategy utilizing epigenetic targeting of neuroblastoma with TERT overexpression.

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Genome-wide BRD4 occupancy upon expression of YFV capsid in Huh-7 cells

Project description:Genome-wide BRD4 occupancy upon expression of YFV capsid in Huh-7 cells

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Genome-wide BRD4 occupancy upon expression of YFV capsid in Huh-7 cells

Project description:We generated genome-wide ChIP-seq binding profiles of BRD4 to analyze the role of YFV capsid lysine residues in the levels of BRD4 on chromatin

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Targeting super-enhancer induced gene expression using novel BRD4 inhibitor OTX015 in preclinical models of MYCN-amplified neuroblastoma

Project description:Bromodomain-containing protein 4 (BRD4) functions as an epigenetic reader and binds to so-called super-enhancer regions of driving oncogenes such as MYC in cancer. We investigated the possibility to target super-enhancer regulated genes in neuroblastoma and in MYCN amplified disease in particular. We used OTX015, the first small-molecule BRD4 inhibitor to enter clinical phase I/II trials in adults, to test the feasibility to specifically target super-enhancer regulated gene-expression in neuroblastoma. BRD4 inhibition lead to significant transcriptional down-regulation of genes that were associated with super-enhancers, supporting the notion that BRD4 preferentially acts at these chromatin sites. BRD4 inhibition not only attenuated MYCN transcription but most significantly affected MYCN-regulated transcriptional programs.

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Genome-wide profiling of SMARCA4 in neuroblastoma cells [ChIP-seq]

Project description:To reveal the genome-wide targets of SWI/SNF complexes in neuroblastoma cells, we performed ChIP-seq of SMARCA4 (BRG1) in IMR-32, KELLY, and SK-N-DZ cells. We used these libraries to examine chromatin occupancy profiling. Analysis of locations reveal that SMARCA4 targets directly regulate sites regulated by the neuroblastoma core regulatory circuitry.

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Genome-wide occupancy of CNBP and SMARCC2 in neuroblastoma cells.

Project description:Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through integrated proteomics and validating studies, we discovered that CNBP physically interacted with SMARCC2 in NB cells. To investigate the mechanisms underlying the functions of CNBP and SMARCC2, we employed the Illumina Novaseq 6000 as a discovery platform to analyze the genome-wide occupancy of CNBP and SMARCC2 on target genes in human IMR-32 cells, while the results were further analyzed with CNBP-regulated target genes. The results showed that CNBP repressed the enrichment of SMARCC2 on 124 target genes, especially those involved in ribosome biogenesis, including BYSL, NOP58, and RRP9. Furthermore, we validated the ChIP-seq results by real-time PCR with high identity. Overall, our results provided fundamental information about the genomic enrichment of CNBP and SMARCC2 in human NB cells, and these findings will help us understand the pathogenesis of NB.

2023-08-07 | GSE215795 | GEO

Genome-wide BRD4, PolII and p65 occupancy as well as chromatin modifications in bone marrow derived macrophages from BRD4 conditional KO mice

Project description:We are reporting here genome wide distribution of BRD4 in bone marrow derived macrophages at steady state level and in reponse to LPS stimulation. In both condition, BRD4 distribution was found to be widespread in intragenic as well as intergenic regions with enrichment specifically near TSS. Characteristically BRD4 signal were highly enriched on enhancers of some active genes and hence were classified as BRD4 rich super-enhancers (>12kb long stretches). Super-enhancers are formed, in some instances by redistribution of BRD4 on LPS stimulated genes. BRD4 binding well correlated PolII binding at the chromatin acetylated at H3K27, H3K9 and H4tetraK. Interestingly many LPS induced BRD4 independent genes, despite BRD4 loss in the KO, maintained PolII binding at the chromatin enriched with acetylated lysines at H3K27, H3K9 and H4tetraK. Additionally among some BRD4 independent LPS inducible genes we detected stronger p65 enrichment in the KO. In contrast, P65 binding was not detected in BRD4 dependent genes. These observations provided evidence of plasticity of epigenetic changes in retaining inflammatory reponses in macrophages.

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Genome-wide Association Study of Neuroblastoma

Project description:Genome-wide Association Study of Neuroblastoma

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