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Brd4 and CEBPB binding profiles with or without BET inhibitor JQ1 in human leukemia OCI-AML3 cells

ABSTRACT: Brd4 and CEBPB binding profiles with or without BET inhibitor JQ1 in human leukemia OCI-AML3 cells

PROVIDER: PRJNA413745 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6151410.fastq.gz	Fastqsanger.gz
	SRR6151411.fastq.gz	Fastqsanger.gz
	SRR6151412.fastq.gz	Fastqsanger.gz
	SRR6151413.fastq.gz	Fastqsanger.gz
	SRR6151408.fastq.gz	Fastqsanger.gz

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Brd4 and CEBPB binding profiles with or without BET inhibitor JQ1 in human leukemia OCI-AML3 cells

Project description:Brd4 is the best characterized member of the bromo- and extra-terminal (BET) domain family of proteins and has been widely studied in tumor-associated transcriptional programs. Here we show that activation of Brd4 is associated with the presence of autophagy in NPMc+ and MLL AML cells. Brd4 binds to the promoters of Atg 3, 7 and CEBPb, and expression of these genes is markedly reduced by inhibitors of Brd4, as well as by Brd4-shRNA and CEBPb depletion. Inhibitors of Brd4 also dramatically suppress the transcription of Keap1, thereby increasing the expression of anti-oxidant genes through the Nrf2 pathway. We conclude that Brd4 plays a significant role in autophagy activation through the direct transcriptional regulation of genes essential for autophagy, as well as through the Keap1-Nrf2 axis in NPMc+ and MLL-fusion AML cells.

2017-10-11 | GSE104745 | GEO

Effect of PROTAC-mediated BRD4 degradation in acute myeloid leukemia [OCI-AML3]

Project description:BRD4, a member of the BET family of histone readers, binds to acetylated lysine of histone H3 and promotes assembly of super-enhancer complexes that drive expression of key oncogenes in acute myeloid leukemia (AML) and other cancers. ARV-825 is a proteolysis-targeting chimera (PROTAC) that targets BRD4 for CRBN-mediated ubiquitination and degradation. We treated the AML cell line OCI-AML3, as well as primary tumor cells from a case of AML, with ARV-825 in vitro. At low concentrations, ARV-825 caused profound and sustained reduction in BRD4 protein levels. This caused reduction in transcription of key genes including MYC, anti-apoptotic BCL2 and BCLXL, PIM1, and CD44. Downstream effects included loss of CXCR4 surface expression and mitochondrial respiration; increased reactive oxygen species; toxicity to AML cells in vitro; and efficacy vs. OCI-AML3 cells in a mouse model of AML.

2019-10-01 | GSE101380 | GEO

OCI-AML3 Tn5 Proximity labeling

Project description:Proximity labeling around Tn5 on OCI-AML3 cells, with (plus) and without Tn5.

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Human OCI-AML3 cells: Control vs. Atg5-shRNA or NPM1-shRNA inducibly expressed

Project description:Transcriptional profiling of human OCI-AML3 cells stably expressing inducibly Atg5 shRNA or NPM1-shRNA Goal was to determine the effects of knockdown of Atg5 or NPM1 on global ES gene expression of human Leukemia OCI-AML3 cells.

2018-03-31 | GSE66904 | GEO

Effects of BRD4 inhibition in AML

Project description:The BET (bromodomain and extra terminal) protein family members including BRD4 bind to acetylated lysines on histones and regulate the expression of important oncogenes, e.g., MYC and BCL2. Here we demonstrate the sensitizing effects of the histone hyperacetylation inducing pan-histone deacetylase inhibitor (HDI) panobinostat (PS) on human AML blast progenitor cells (BPCs) to the BET protein inhibitor JQ1. Treatment with JQ1 but not its inactive enantiomer (R-JQ1) was highly lethal against AML BPCs expressing mutant NPM1c+ with or without co-expression of FLT3-ITD, or AML expressing MLL fusion oncoprotein. JQ1 treatment reduced binding of BRD4 and RNA polymerase II to the DNA of MYC and BCL2, and reduced their levels in the AML cells. Co-treatment with JQ1 and the HDAC inhibitor panobinostat (PS) synergistically induced apoptosis of the AML BPCs, but not of normal CD34+ hematopoietic progenitor cells. This was associated with greater attenuation of MYC and BCL2, while increasing p21, BIM and cleaved PARP levels in the AML BPCs. Co-treatment with JQ1 and PS significantly improved the survival of the NOD/SCID mice engrafted with OCI-AML3 or MOLM13 cells (p < 0.01). These findings highlight co-treatment with a BRD4 antagonist and an HDI as a potentially efficacious therapy of AML. Two samples were analyzed (untreated cells, cells treated with JQ1)

2014-01-01 | E-GEOD-51950 | biostudies-arrayexpress

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Project description:Human acute myeloid leukemia cell lines OCI-AML2 and OCI-AML3 were used in a CRISPR/Cas9-mediated approach to specifically target DDX3X’s gene sequences encoding the RNA binding domain of the helicase. DDX3X RNA binding domain is bipartite in the two halves of the helicase core. sgRNAs were designed to target both halves of the domain (named RNA binding domain A and B – RBDA and RBDB). We performed RNA-seq to observe the gene expression changes in both OCI-AML2 and OCI-AML3 cell lines following the not-combined CRISPR/Cas9 –mediated targeting of both regions of the DDX3X RNA binding domain. Control CRISPR/Cas9 performed with no sgRNA expressing vector (named “empty vector”) was performed in both cell lines. The latter condition was used as a control for gene expression changes analysis, for each cell line.

2019-11-23 | E-MTAB-6241 | biostudies-arrayexpress

In vivo effects of localization and/or CXCR4 inhibition on gene expression profiles of OCI-AML3 cells

Project description:OCI-AML3, a human acute myeloid leukemia cell line, was inoculated into NOD/SCID/IL-2rγnull (NSG) mice. After engraftment and leukemic expansion were documented, mice were divided into 3 groups: control, or treatment for 24 or 72 hours with daily injections of LY2510294, a CXCR4-inhibitory peptide. OCI-AML3 cells were isolated from peripheral blood (PB), bone marrow (BM), or spleen (SP) for gene expression profiling (GEP).

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GLUT3 salvage with vitamin C treatment altered gene expression landscape of OCI-AML3

Project description:To investigate the GLUT3 salvage-induced transcriptome changes, we performed RNA-seq on the SLC2A3 overexpressed and the empty control OCI-AML3 cell lines treated with 250 µM of vitamin C.

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Project description:To identify molecular effects of the dual PI3K/mTOR inhibitor omipalisib (GSK2126458), we applied gene expression profiling in human leukemic cell lines OCI-AML3 using Whole Transcriptome Shotgun Sequencing (RNA-seq). After OCI-AML3 cell were treated with 50 nM omipalisib for 24 h, differentially expressed genes (DEGs) of 1245 genes upregulated and 811 were downregulated were found compared with vehicle group. Down-regulated genes enriched in cell cycle, DNA metabolic process, PI3K/AKT/mTOR signaling, MYC pathway, E2F pathway, Gly, Ser and Thr metabolism, Cys and Met metabolism, carbon metabolism, oxidative phosphorylation, mitochondrial biogenesis and respiratory electron transporter chain.

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