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

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

PROVIDER: PRJNA788137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17205246_1.fastq.gz	Fastqsanger.gz
	SRR17205246_2.fastq.gz	Fastqsanger.gz
	SRR17205247_1.fastq.gz	Fastqsanger.gz
	SRR17205247_2.fastq.gz	Fastqsanger.gz
	SRR17205248_1.fastq.gz	Fastqsanger.gz

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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

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.

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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.

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SMARCA4 Phosphorilation inhibition

Project description:Cyclin-Dependent Kinase 9 (CDK9) as part of the PTEFb complex promotes transcriptional elongation and high-level gene expression. We now report that, paradoxically, CDK9 is also essential for maintaining gene silencing at heterochromatic loci. Through a live cell screen, we discovered that CDK9 inhibition reactivates epigenetically silenced genes in cancer, leading to restored tumor suppressor gene expression and cell differentiation, along with activation of endogenous retrovirus (ERV) genes. CDK9 inhibition maintains gene silencing directly through phosphorylation of the SWI/SNF protein SMARCA4 and indirectly through HP1α activation. Based on gene activation, we developed the highly selective and 2 potent CDK9 inhibitor MC180295 (IC50 =5.1nM) that has broad anti-cancer activity in-vitro and is effective in in-vivo cancer models. Additionally, CDK9 inhibition synergizes with the immune checkpoint inhibitor α-PD-1 in vivo, making it an excellent target for epigenetic therapy of cancer.

2023-06-13 | PXD008040 | Pride

SMARCA4-dependent regulation of chromatin and transcription in neuroblastoma

Project description:SMARCA4-dependent regulation of chromatin and transcription in neuroblastoma

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

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

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BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways

Project description:Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin- dependent regulator of chromatin, subfamily a, member 4 (SMARCA4/BRG1) was consistently upregulated in advanced stages of NB, with high BRG1 levels being indicative of poor outcome. Loss-of-function experiments in vitro and in vivo showed that BRG1 is essential for the proliferation of NB cells. Furthermore, whole genome transcriptome analysis revealed that BRG1 controls the expression of key elements of oncogenic pathways such as PI3K/AKT and BCL2, which offers a promising new combination therapy for high-risk NB Non-silencing control (NSC) or shBRG1 lentiviral vectors were transduced in the Neuroblastoma cell lines SK-N-BE(2) by triplicate. 48h post-infection, total RNA was extracted

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2015-07-12 | E-GEOD-67920 | biostudies-arrayexpress

Transcriptional effects of dominant-negative G784E Smarca4 mutation in mouse embryonic stem cells [RNA-seq]

Project description:We investigated transcriptomic effects of a Smarca4 ATPase mutant observed in primary tumors and cancer cell lines. Heterozygous expression of G784E Smarca4 mutant led to transcriptional changes compared to cells expressing only wild-type Smarca4.

2017-10-22 | GSE98469 | GEO

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

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

| PRJNA788139 | ENA