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

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

PROVIDER: PRJNA777427 | ENA |

REPOSITORIES: ENA

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

Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced gene expression data upon treatment with NTX-301 or decitabine (DAC) in MV4-11 cell line.

2022-04-20 | GSE187285 | GEO

DNA methylation profiling upon treatment with NTX-301 or decitabine in AML cells

Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced methylome data upon treatment with NTX-301 or decitabine (DAC) in MV4-11 cell line.

2022-11-30 | GSE187291 | GEO

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.

2015-07-12 | E-GEOD-67920 | biostudies-arrayexpress

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

2015-07-12 | GSE67920 | GEO

Gene expression profiling upon treatment with NTX-301

2022-04-20 | GSE188392 | GEO

Aurora-A interactome in MV4-11 cells

Project description:To determine interactors of Aurora-A, HA tagged Aurora-A was immunoprecipitated from MV4-11 cells stably expressing HA tagged Aurora-A wild type and compared to MV4-11 cells expressing empty vector.

2020-09-28 | PXD019684 | Pride

Gene expression profiling upon treatment with NTX-301

Project description:Gene expression profiling upon treatment with NTX-301

| PRJNA778722 | ENA

CD36 impacts the expression of genes in MV4-11 cells

Project description:CD36 impacts the expression of genes in MV4-11 cells

2024-05-14 | GSE209783 | GEO

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.

2021-02-12 | GSE166621 | GEO

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.

2016-08-01 | E-GEOD-74666 | biostudies-arrayexpress

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