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Differential expression analysis from MV4-11 cells treated with or without APTO-253 for 6 hours.

ABSTRACT: Differential expression analysis from MV4-11 cells treated with or without APTO-253 for 6 hours.

PROVIDER: PRJNA438668 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6847835.fastq.gz	Fastqsanger.gz
	SRR6847836.fastq.gz	Fastqsanger.gz
	SRR6847837.fastq.gz	Fastqsanger.gz
	SRR6847838.fastq.gz	Fastqsanger.gz

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Differential expression analysis from MV4-11 cells treated with or without APTO-253 for 6 hours.

Project description:RNA-seq and differential gene expression analysis were used to detect specific genes and pathways either up or down regulated in the AML cell line MV4-11 after treatment with novel small molecule APTO-253. The aim of the analysis was to elucidate genes or pathways that are key to the celular phenotype of APTO-253 mechanism of action in killing AML cells. W detected an effect on MYCexpression, DNA damage and cell stress response pathwyas and cell cycle arrest.

2018-05-15 | GSE111949 | GEO

Aurora-A interactome in MV4-11 cells

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CD36 impacts the expression of genes in MV4-11 cells

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Transcriptome profile of MV4-11 cells with FEV deficiency

Project description:Enhanced homing and uncontrolled expansion are the characteristics of AML cells. We identified a transcription factor FEV (fifth Ewing variant) as the regulator. To assess the regulation mechanisms, FEV expression was knocked down in AML cell line MV4-11 cells using shRNA. MV4-11 cells transduced with non-silencing control (NC), FEV shRNA (shFEV) were cultured for 3 days and sorted by FACS. The cells were collected and total RNA was isolated by the Trizol kit (Takara Bio, Otsu, Japan) according to manufacturer’s protocol. High-throughput RNA sequencing (RNA-seq) was performed by Illumina HiSeq 2500 (Illumina, San Diego, CA) at CapitalBio Corporation (Beijing, China). Differentially expressed genes were analysed between the two groups.

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Gene expression profiling upon treatment with NTX-301 in MV4-11

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Comparation the mRNA Expression Profile of the MV4-11 Sorafenib Resistant Cells and the Parental Cells

Project description:Our gene set analysis of MV4-11-R versus MV4-11 indicated decreased depolarization of mitochondria and mitochondrial membrane, mitochondrial dysfunction and anti-apoptosis as other top ranked molecular or cellular functions of differential gene sets. expression of most genes encoding glycolytic enzymes was up-regulated in MV4-11-R cells we revealed a metabolic alteration in sorafenib-resistant cell lines with mitochondrial respiration deficiency, leading to substantial decrease of mitochondria-derived ATP generation and a significant increase in glycolytic activity to maintain sufficient ATP production. Our study revealed a metabolic signature of sorafenib resistance and indicated that increase of glycolytic activity including upregulation of major glycolytic enzymes may be viewed as a marker for early detection of sorafenib resistance in AML patients with FLT3/ITD mutation and glycolytic inhibitors warrant further investigation as alternative therapeutic agents for sorafenib-resistant cells Sorafenib resistant cells MV411-R VS. parental MV4-11 cells. Biological replicates: 3 control replicates, 3 treated replicates.

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Gene expression changes in MV4-11 cells upon SMARCA4 knock-down and PFI-3 treatment

Project description:Pharmacological inhibition of the SMARCA4 bromodomain inhibited human leukemic cell proliferation, phenocopying SMARCA4 knockdown in these cells. We performed microarray analysis of global gene expression changes in MV4-11 cells after 6 days of PFI-3 treatment and after SMARCA4 knock-down. With this analysis we identified several genes whose expression was similarly up- or down-regulated upon inhibitor treatment and SMARCA4 depletion. Human acute monocytic leukemia cells (MV4-11, ACC 102) were lentivirally transduced with shRNA taregting SMARCA4 (KD) or with a negative control shRNA (Scr). In a parallel experiment MV4-11 cells were treated for 6 days with 10 uM PFI-3, which is SMARCA4, SMARCA2 and PBRM1 bromodomain inhibitor, or DMSO as a negative control. All sample types were prepared in triplicates.

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