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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

ABSTRACT: Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

PROVIDER: PRJNA679614 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13088783_1.fastq.gz	Fastqsanger.gz
	SRR13088783_2.fastq.gz	Fastqsanger.gz
	SRR13088784_1.fastq.gz	Fastqsanger.gz
	SRR13088784_2.fastq.gz	Fastqsanger.gz
	SRR13088785_1.fastq.gz	Fastqsanger.gz

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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

Project description:We examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Wild type and SMARCA4 silenced cells were subjected to ATAC-seq in the absence or presence of RSV infection. Cells were infected for 0 or 24 h prior to RNA seq.

2021-01-01 | GSE161847 | GEO

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

Project description:We examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Wild type and SMARCA4 silenced cells were subjected to short read illumina RNA Seq in the absence or presence of RSV infection. Cells were infected for 0, 16 h or 24 h prior to RNA seq.

2021-01-01 | GSE161846 | GEO

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

| PRJNA679613 | ENA

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

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siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-01 | GSE161849 | GEO

Role of Specialized Composition of SWI/SNF Complexes in Prostate Cancer Lineage Plasticity

Project description:Advanced prostate cancer initially responds to hormonal treatment, but ultimately becomes resistant and requires more potent therapies. One mechanism of resistance seen in 10% of these patients is through lineage plasticity, which manifests in a partial or complete small cell or neuroendocrine prostate cancer (NEPC) phenotype. Here, we investigate the role of the mammalian SWI/SNF chromatin remodeling complex in NEPC. Using large patient datasets, patient-derived organoids and cancer cell lines, we identify SWI/SNF subunits that are deregulated in NEPC, demonstrate that SMARCA4 (BRG1) overexpression is associated with aggressive disease and that SMARCA4 depletion impairs prostate cancer cell growth. We also show that SWI/SNF complexes interact with different lineage-specific factors in prostate adenocarcinoma and in NEPC cells, and that induction of lineage plasticity through depletion of REST is accompanied by changes in SWI/SNF genome occupancy. These data suggest a specific role for mSWI/SNF complexes in therapy-related lineage plasticity, which may be relevant for other solid tumors.

2020-11-04 | PXD016861 | Pride

The SWI/SNF complex regulates the expression of miR-222, a tumor suppressor microRNA in lung adenocarcinoma

Project description:Mammalian SWI/SNF complexes are considered as key epigenetic regulators and they are recurrently mutated in many types of cancer. Most of the studies of these chromatin remodeling complexes are focused on their role in regulating protein-coding genes. However, here we show that the SWI/SNF complex is able to control the expression of microRNAs. We used a SMARCA4-deficient model of lung adenocarcinoma where we could track changes of the miRNome upon SMARCA4 restoration. We found that exogenous SMARCA4 was successfully incorporated into endogenous SWI/SNF complexes and that these SMARCA4-SWI/SNF complexes induced significant changes in the expression of cancer-related microRNAs. The most significantly dysregulated miRNA was miR-222, whose expression was promoted by SMARCA4-SWI/SNF complexes but not by SMARCA2-SWI/SNF complexes via their direct binding to a miR-222 enhancer region. Importantly, miR-222 expression decreased cell viability and impaired cell clonogenicity, phenocopying the tumor-suppressor role of the SMARCA4-SWI/SNF complex in lung cancer. Finally, we showed that the miR-222 enhancer does not interact with any cancer-related protein-coding genes, supporting that its tumor suppressor effect may be exerted via miR-222. Overall, this study highlights the relevant role of the SWI/SNF complex in regulating the expression of the non-coding genome.

2021-07-20 | GSE167140 | GEO

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [HiChIP-Seq]

Project description:This study profiles chromatin accessibility, gene expresison, transcription factor binding, and three-dimensional DNA-DNA contact changes upon rapid SWI/SNF ATPase inactivation in prostate cancer cells. SWI/SNF ATPases activity was disabled using a novel PROTAC degrader compound targeting the SMARCA2, SMARCA4 and PBRM1 subunits of the SWI/SNF remodeling complex.

2021-10-28 | GSE171591 | GEO

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [ChIP-Seq]

2021-10-28 | GSE171589 | GEO