Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional effects of SWI/SNF inhibition in acute myeloid leukemia cells [RNA-seq]

ABSTRACT: To reveal the effects of SWI/SNF inhibition in KMT2Ar leukemic cells, we performed RNA-seq in THP-1, MOLM-13, and MV-4-11 cells, and compared the effects of BRM014 with DMSO vehicle control. We also compared these effects to PMA-induced differentiation in THP-1 cells, as well as treatment with the PU.1 inhibitor DB2313. Analysis of transcripts reveal that SMARCA4 inhibition promotes differentiation, down-regulation of MYC and its target genes, and reduced expression of CD44, consistent with loss of self-renewal.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190722 | GEO | 2023/01/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DNA accessibility sites requiring SWI/SNF activity in AML [ATAC-seq]

Project description:To reveal the genome-wide targets of SWI/SNF complexes in AML cells, we performed ATAC-seq in THP-1, MOLM-13, and MV-4-11 cells with or without the SWI/SNF ATPase BRM014. Analysis of the locations decreased following 24 or 72 h after addition of BRM014 revealed that SWI/SNF-dependent sites are located at enhancers occupied by PU.1, especially the blood enhancer cluster (BENC), a set of enhancers that drives expression of MYC.

2023-01-10 | GSE190721 | GEO

Chromatin occupancy profiling of AML transcription factors upon SWI/SNF inhibition [ChIP-seq]

Project description:To reveal the effects of SWI/SNF inhibition on genome-wide transcription factor occupancy in AML cells, we performed ChIP-seq in THP-1 cells, and compared the effects of BRM014 with DMSO vehicle control. We also examined the effects of SMARCA4 chromatin targeting via treatment with the PU.1 inhibitor DB2313. Analysis of genome-wide occupancy by ChIP-seq reveals that SWI/SNF inhibition impairs PU.1-directed enhancer programs in AML cells.

2023-01-10 | GSE217171 | GEO

Transcriptional effects of SMARCA4 inhibition on neuroblastoma cells [4sU RNA-seq]

Project description:To reveal fast-acting transcriptional effects of SWI/SNF inhibition in neuroblastoma cells, we performed 4sU metabolic labeling followed by RNA-seq in IMR-32, KELLY, and SK-N-DZ cells and compared the effects of BRM014 with DMSO vehicle control. We also compared these effects to auxin-induced degradation of SMARCA4 in engineered cells with the minimal auxin-induced degron (SMARCA4-mAID). Analysis of transcripts reveal that SMARCA4 inhibition leads to suppression of transcripts involved in the G1 checkpoint.

2023-10-24 | GSE190708 | GEO

Transcriptional changes in bone marrow cells upon SWI/SNF inhibition [scRNA-seq]

Project description:Despite significant therapeutic potential of SWI/SNF inhibition therapy, the off-tumor effects of SWI/SNF inhibition remain largely unknown. Here, we quantify the effects of the dual SWI/SNF ATPase inhibitor BRM014 on bone marrow cells in mice. We identify lineage-dependent effects on the B and monocyte lineages within the bone marrow.

2023-01-10 | GSE205571 | GEO

DNA accessibility sites requiring SMARCA4 activity in neuroblastoma cells [ATAC-seq]

Project description:To reveal the genome-wide targets of SWI/SNF complexes in neuroblastoma cells, we performed ATAC-seq in IMR-32 cells with or without SMARCA4 inactivation. To identify changes in DNA accessibility following SMARCA4 inactivation, we used either the small-molecule catalytic inhibitor BRM014, auxin-induced degradation of IMR-32 cells engineered with SMARCA4 tagged to the minimal auxin-induced degron (SMARCA4-mAID), or the corresponding vehicle controls. Analysis of these locations reveal that SMARCA4-dependent sites are located at enhancers used by the neuroblastoma core regulatory circuitry.

2023-10-24 | GSE190706 | GEO

Epigenome analysis of parental and ABT-199 resistant AML cell lines

Project description:Genome wide DNA methylation profiling of parental, ABT-199 resistant population, and ABT-199 resistant clones from 3 acute myelogenous leukemia (AML) cell lines (MOLM-13, MV-4-11, OCI-AMLO2). The Illumina Infinium MethylationEPIC Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs from AML cell line samples. Samples include 4 ABT-199 sensitive parental MOLM-13 population samples, 4 ABT-199 resistant MOLM-13 population samples, 3 ABT-199 resistant MOLM-13 S2 clone samples, 3 ABT-199 resistant MOLM-13 S5 clone samples, 4 ABT-199 resistant MOLM-13 S6 clone samples, 3 ABT-199 sensitive parental MV-4-11 population samples, 3 ABT-199 resistant MV-4-11 population samples, 3 ABT-199 sensitive parental OCI-AML2 population samples, 3 ABT-199 resistant OCI-AML2 population samples, 3 ABT-199 resistant OCI-AML2 S1 clone samples, 3 ABT-199 resistant OCI-AML2 S2 clone samples, 3 ABT-199 resistant OCI-AML2 S8 clone samples.

2022-01-12 | GSE193254 | GEO

Changes of DNA accessibility and RNA transcription upon SWI/SNF inhibition in peripheral blood and bone marrow cells [multiome]

Project description:Despite significant therapeutic potential of SWI/SNF inhibition therapy, the off-tumor effects of SWI/SNF inhibition remain largely unknown. Here, we quantify the effects of the dual SWI/SNF ATPase inhibitor BRM014 on peripheral blood (PB) and bone marrow (BM) cells in mice. We identify altered chromatin regulatory mechanisms in B cells and monocytes.

2023-01-10 | GSE205570 | GEO

Pioglitazone competes with EGR1 to suppress PKD1 in Angiotensin II-treated macrophages

Project description:THP-1 cells were differentiated to macrophages with the phorbol 12-myristate 13-acetate (PMA) for a total time of 28 hours. To understand the effects of Angiotensin II (AngII) and of AngII in the presence of the thiazolidinedione pioglitazone (Pio), after 4 hours of PMA-induced differentiation of THP-1 cells (when cells became adherent), the PMA-containing medium was supplemented with AngII (1mg/ml), AngII (1 mg/ml) with Pio (1 uM), or no supplement for another 24 hours. At this time point the cells were harvested, RNA was extracted and used for a microarray-based gene profiling analysis of THP-1 cells, under the three conditions: PMA, AngII and AngII with Pio.

2014-06-01 | E-MTAB-2320 | biostudies-arrayexpress

SWI/SNF-dependent genes are defined by their chromatin landscape [ChRNA-seq]

Project description:The SWI/SNF complex was the first chromatin remodeling machinery discovered. Although it has been extensively investigated, numerous aspects of its regulation and activity are still poorly understood, especially in higher eukaryotes. In mammals, there is not a single SWI/SNF complex (also called BRM or BRG1 associated factors, BAF, complex) but rather a polymorphic family of complexes, with three main subtypes called canonical BAF (cBAF), polybromo-associated BAF (PBAF), and non-canonical BAF (ncBAF), with relatively different specificities. The enzymatic motors of the complexes are two mutually exclusive ATPases of the SNF2 family called BRAHMA (BRM, also called SMARCA2) and BRAHMA RELATED GENE 1 (BRG1, also called SMARCA4). Recently, an specific inhibitor of BRM and BRG1 ATPase activity, called BRM014, has been developed. We have extensively investigated the effect of BRM014 on the transcriptome and the chromatin landscape of non-tumoral normal murine mammary (NMuMG) epithelial cells.

2024-03-08 | GSE226947 | GEO

SWI/SNF-dependent genes are defined by their chromatin landscape [MNase-seq]

2024-03-08 | GSE226950 | GEO