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.
Project description:GSK3685032-induced DNA hypomethylation results in upregulation of largely viral-responsive gene expression pathways and cell death. We identified that loss of RNF4 causes resistance to GSK3685032. We established RNF4 wild type and deficient MV4-11 cells by CRISPR-Cas9 disruption and treated with vehicle or GSK3685032 to determine how RNF4-deficiency impacts GSK3685032-induced gene expression changes
Project description:GSK3685032-induced DNA hypomethylation results in upregulation of largely viral-responsive gene expression pathways and cell death. We identified that loss of RNF4 causes resistance to GSK3685032. We established RNF4 wild type and deficient MV4-11 cells by CRISPR-Cas9 disruption and treated with vehicle or GSK3685032 to determine how RNF4-deficiency impacts GSK3685032-induced gene expression changes
Project description:GSK3685032-induced DNA hypomethylation results in upregulation of largely viral-responsive gene expression pathways and cell death. We identified that loss of RNF4 causes resistance to GSK3685032. We established RNF4 wild type and deficient MV4-11 cells by CRISPR-Cas9 disruption and treated with vehicle or GSK3685032 to determine how RNF4-deficiency impacts GSK3685032-induced gene expression changes
Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to explore CUT-TAG results of LDB1 in MV4-11 cell line.
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.
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.
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.
