Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin profiling following SWI/SNF inhibition in neuroblastoma cells [ChIP-seq]

ABSTRACT: To assess the genome-wide effects of SWI/SNF activity in MYCN-amplified neuroblastoma cells, we performed ChIP-seq in IMR-32 cells treated with either DMSO or the SWI/SNF inhibitor BRM014. Pronounced loss of chromatin occupancy was observed for members of the neuroblastoma core regulatory circuitry within 1 hour.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206310 | GEO | 2023/10/24

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 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

Genome-wide profiling of SMARCA4 in neuroblastoma cells [ChIP-seq]

Project description:To reveal the genome-wide targets of SWI/SNF complexes in neuroblastoma cells, we performed ChIP-seq of SMARCA4 (BRG1) in IMR-32, KELLY, and SK-N-DZ cells. We used these libraries to examine chromatin occupancy profiling. Analysis of locations reveal that SMARCA4 targets directly regulate sites regulated by the neuroblastoma core regulatory circuitry.

2023-10-24 | GSE190707 | GEO

Targeting SWI/SNF ATPases reduces cell invasiveness and plasticity in core transcription factors-addicted neuroblastoma

Project description:Neuroblastoma (NB) comprises mesenchymal (MES) and adrenergic (ADRN) subtypes, and the cell identity is determined by core transcription factors (TFs). However, the binding mechanism of these TFs to DNA and the epigenetic mechanisms governing NB plasticity remain unclear. In this study, we investigated the impact of targeting SWI/SNF ATPases with SMARCA2/4 dual degraders on NB cells. Our results revealed that depletion of SWI/SNF ATPases compacted cis-regulatory elements, diminished enhancer activity, and displaced core TFs (MYCN, HAND2, PHOX2B, and GATA3) from DNA, suppressing transcriptional programs linked to plasticity and invasiveness. These findings underscore the pivotal role of SWI/SNF ATPases in driving NB progression, positioning them as promising therapeutic targets.

2024-08-28 | GSE240724 | GEO

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

Targeting SWI/SNF ATPases reduces cell invasiveness and plasticity in core transcription factors-addicted neuroblastoma [ChIP-seq]

2024-08-28 | GSE240589 | GEO

Targeting SWI/SNF ATPases reduces cell invasiveness and plasticity in core transcription factors-addicted neuroblastoma [RNA-seq]

2024-08-28 | GSE240590 | GEO

Targeting SWI/SNF ATPases reduces cell invasiveness and plasticity in core transcription factors-addicted neuroblastoma [ATAC-seq]

2024-08-28 | GSE240588 | 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

Targeting SWI/SNF ATPases reduces neuroblastoma cell plasticity

Project description:Targeting SWI/SNF ATPases reduces neuroblastoma cell plasticity

| PRJNA1004275 | ENA