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RNA-seq analysis of SCC1 cells after JQ1, I-BET and/or INF-r treatment

ABSTRACT: RNA-seq analysis of SCC1 cells after JQ1, I-BET and/or INF-r treatment

PROVIDER: PRJNA689302 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13344385.fastq.gz	Fastqsanger.gz
	SRR13344386.fastq.gz	Fastqsanger.gz
	SRR13344387.fastq.gz	Fastqsanger.gz
	SRR13344388.fastq.gz	Fastqsanger.gz
	SRR13344389.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of SCC1 cells after JQ1, I-BET and/or INF-r treatment

Project description:In order to examine how BET inhibition affects the gene transcriptome in HNSCC cells, we performed RNA-sequencing in SCC1 cells treated with JQ1, I-BET, and/or INF-r.

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ChIP-seq analysis of BRD4, MED1 and P65 in SCC1 cells after JQ1 treatment

Project description:To explore genome-wide alteration of BRD4, MED1, p65 and H3K27Ac during BET inhibition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of the MED1, BRD4, p65 and H3K27ac following JQ1 treatment. BET inhibition by JQ1 led to dramatically loss of the recruitment of MED1, BRD4 and p65 at a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

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Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity. DV90 cells (JQ1 sensitive non-small cell lung cancer cell line) were treated with 135 nM (IC50) or 785 nM (IC90) of JQ1 for 4h and 24h. DMSO treated controls served as reference and at least four replicates per condition were collected. RNA was extracted and hybridized to Affymetrix HuGene-2.1ST microarrays to identify treatment induced transcriptional changes.

2016-03-31 | E-GEOD-75960 | biostudies-arrayexpress

Transcripitional profiling of Huh7 cells after MAT2A inhibitor (FIDAS-5) or BET bromodomain inhibitor (JQ1) treatment

Project description:RNA-seq analysis of Huh7 cells after MAT2A inhibitor (FIDAS-5) or BET bromodomain inhibitor (JQ1) treatment. The analysis revealed that inhibition of MAT2A or BET factors suppresses the expression of genes regulating cell cycle progression and additional cellular programs.

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Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

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CAGE profiling after treatment with JQ1 BET inhibitor in lung cancer cell line.

Project description:The bromodomain and extra-terminal domain (BET) proteins are promising drug targets for cancer and immune diseases. However, BET inhibition effects have been studied more in the context of bromodomain-containing protein 4 (BRD4) than BRD2, and the BET protein association to histone H4-hyperacetylated chromatin is not understood at the genome-wide level. Here, we report transcription start site (TSS)-resolution integrative analyses of ChIP-seq and transcriptome profiles in human non-small cell lung cancer (NSCLC) cell line H23. We show that di-acetylation at K5 and K8 of histone H4 (H4K5acK8ac) co-localizes with H3K27ac and BRD2 in the majority of active enhancers and promoters, where BRD2 has a stronger association with H4K5acK8ac than H3K27ac. Although BET inhibition by JQ1 led to complete reduction of BRD2 binding to chromatin, only local changes of H4K5acK8ac levels were observed, suggesting that recruitment of BRD2 does not influence global histone H4 hyperacetylation levels. This finding supports a model in which recruitment of BET proteins via histone H4 hyperacetylation is predominant over hyperacetylation of histone H4 by BET protein-associated acetyltransferases. In addition, we found a remarkable number of BRD2-bound genes, including MYC and its downstream target genes, were transcriptionally upregulated upon JQ1 treatment. Using BRD2-enriched sites and transcriptional activity analysis, we identified candidate transcription factors potentially involved in the JQ1 response in BRD2-dependent and independent manner.

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| PRJNA544484 | ENA