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NCI-H1688 cells treated with natural compounds(sanguinarine chloride, cepharanthine and evodiamine), or (+)-JQ-1, or panobinostat, or sanguinarine chloride in combination with panobinostat or (+)-JQ-1.

ABSTRACT: NCI-H1688 cells treated with natural compounds(sanguinarine chloride, cepharanthine and evodiamine), or (+)-JQ-1, or panobinostat, or sanguinarine chloride in combination with panobinostat or (+)-JQ-1.

PROVIDER: PRJNA757981 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15618928_1.fastq.gz	Fastqsanger.gz
	SRR15618928_2.fastq.gz	Fastqsanger.gz
	SRR15618929_1.fastq.gz	Fastqsanger.gz
	SRR15618929_2.fastq.gz	Fastqsanger.gz
	SRR15618930_1.fastq.gz	Fastqsanger.gz

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NCI-H1688 cells treated with natural compounds(sanguinarine chloride, cepharanthine and evodiamine), or (+)-JQ-1, or panobinostat, or sanguinarine chloride in combination with panobinostat or (+)-JQ-1.

Project description:Purpose: we used next generation sequencing to analyze gene expression profiles of NCI-H1688 treated with different drugs and elaborated the combinatorial effect of sanguinarine chloride and panobinostat or (+)-JQ-1.The goals of this study are to compare the drug effect and find out the resonally synergistic effects in NCI-H1688.

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Differential gene expression in neuroblastoma cells after treatment with vehicle control, JQ1, panobinostat, or combination of JQ1 and panobinostat

Project description:The bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects We analyzed whether JQ1 and panobinostat synergistically modulate gene expression Neuroblastoma SK-N-BE(2) cells were treated with vehicle control, 1 microM JQ1, 10 nM panobinostat, or combination of JQ1 and panobinostat for 6 hours, and subjected to differential gene expression studies with Affymetrix microarrays.

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Identification of microRNA expression patterns in human myofibroblasts with/without the JQ-1 treatment and/or TGF-b

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease that normal parenchyma is progressively replaced by fibrotic foci comprised of myofibroblasts, active differentiated fibroblasts. IPF has an overall poor prognosis with median survival ranging from 2.5 to 3.5 years. The underlying disease mechanisms in IPF are largely unknown, and there is still no effective drug that prolongs survival of patients with IPF. It has been known that JQ-1, a BET bromodomain inhibitor, prevents TGF-β-mediated fibroblast to myofibroblast differentiation. Moreover, JQ-1 modulates miRNAs expression in various types of cancer cell. In this study, to gain understanding of the relationship between miRNAs expression and the effect of JQ-1 on the dedifferentiation of established myofibroblast, we investigated miRNA profiles in human myofibroblasts with/without the JQ-1 treatment and/or TGF- using miRNA microarray assay.

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Comprehensive transcriptome analysis of human myofibroblasts with/without the JQ-1 treatment [mRNA]

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease that normal parenchyma is progressively replaced by fibrotic foci comprised of myofibroblasts, active differentiated fibroblasts. IPF has an overall poor prognosis with median survival ranging from 2.5 to 3.5 years. The underlying disease mechanisms in IPF are largely unknown, and there is still no effective drug that prolongs survival of patients with IPF. It has been known that JQ-1, a BET bromodomain inhibitor, prevents TGF-β-mediated fibroblast to myofibroblast differentiation. In this study, to obtain a better understanding of the molecular mechanisms underlying the effect of JQ-1 treatment on the dedifferentiation of established myofibroblasts, we performed comparative transcriptome analysis using the high-throughput RNA-seq. The CLC Genomic Workbench software was used to screen the differentially expressed transcripts. A total of 4,155 genes with a significantly differential expression in the JQ-1 treatment group as compared with the control group.

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