Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic Silencing of LTR12C family in OCI-AML3

ABSTRACT: Chromatin accessibility at LTR12C family has been shown to b required to maintain stemness properties in leukemic stem cells. Here using CRISPRi epigenetic silencing strategy, we targetted LTR12C family in OCI-AML3 cell line. Our ATAC-seq and CUT&RUN data demonstrate efficient targeting and silencing of entire family using only 4 sgRNAs. Epigenetic silencing of this family leads to slower growth in targeted OCI-AML3 cells compared to control cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE288771 | GEO | 2025/03/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Epigenetic Silencing of LTR12C family in OCI-AML3

Project description:Epigenetic Silencing of LTR12C family in OCI-AML3

| PRJNA1219225 | ENA

RNA-seq expression profiling of OCI-AML2 and OCI-AML3 cells upon CRISPR/Cas9 –mediated disruption of DDX3X RNA binding domain

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

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

Profiling H3K4me3, H3K4me1, H3K9ac and H3K27ac in OCI-AML3 cells

Project description:OCI-AML3 Acute myeloid leukemia cell line was used for ChIP-sequencing profiling of H3K4me3, H3K4me1, H3K9ac and H3K27ac histone post-translational modifications to identify active promoter and enhancer regions.

2022-04-04 | GSE199964 | 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

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).

2015-06-03 | GSE64623 | GEO

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.

2023-04-25 | GSE216576 | GEO

Effect of omipalisib on transcriptome and signaling pathways in leukemic cell line OCI-AML3

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.

2023-09-15 | GSE224155 | GEO

RNA-seq Analysis of OCI-AML3 Cells Treated with Different Compounds

Project description:Acute myeloid leukemia (AML) remains a challenging hematologic malignancy, necessitating the exploration of novel treatment strategies. In this study, we investigated the effects of all-trans retinoic acid (ATRA), AM80, and their combination treatments with GSK-LSD1 and MB3 on gene expression in OCI-AML3 cells.

2025-02-01 | GSE256476 | GEO

Trancriptome profiling of human OCI-AML3 AML cell line stably transfected by pMEP4-Empty or pMEP4-RhoH plasmids, respectively.

Project description:Transcriptome profiling of Human OCI-AML3 cell line with low RhoH expression, stably transfected either by Empty or by RhoH sur-expressing vectors.

2020-08-03 | GSE138479 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data