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Transcriptome analysis of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation

ABSTRACT: Transcriptome analysis of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation

PROVIDER: PRJNA475578 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7290300.fastq.gz	Fastqsanger.gz
	SRR7290297.fastq.gz	Fastqsanger.gz
	SRR7290298.fastq.gz	Fastqsanger.gz
	SRR7290299.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation

Project description:We conduct transcriptome comparison of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation to gain genomic insights on the biological processes that BRG1 is involved in depend on PTEN deletion. Through unsupervised cluster analysis of differentially expressed genes (DEGs), we found the expressions of 5489 genes were significantly altered in PTEN/BRG1 double knockdown cells, whereas they remained consistent or opposite pattern in control, BRG1-KD and PTEN-KD cells. Differential principal component analysis (PCA) suggested ablation of BRG1 in PTEN-depleted cells forced the cells undergoing a distinct transcriptome as compared to the others. In keeping with these findings, KEGG-DEGs relationship network indicated BRG1 loss in PTEN-deficient cells significantly altered the process related to “Prostate cancer”, “Cell cycle”, “Cell motility” and etc.

2019-01-14 | GSE115616 | GEO

Compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells by ATAC-Seq

Project description:Transposase-accessible chromatin using sequencing (ATAC-seq) assay was performed to compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells. Ablation of BRG1 in PTEN-depleted cells preferentially led to the reductions of OCR at enhancers, but not promoter regions.

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BRG1 occupancy profiling by high throughput sequencing from control and PTEN knockdown 22RV-1 cells

Project description:To identify the downstream targets and pathways mediated by BRG1, chromatin immunoprecipitation followed by sequencing (ChIP–seq) was performed in control and PTEN-knockdown 22RV-1 cells. Total 6279 genes showed the enhanced BRG1 occupancies in PTEN-knockdown cells as compared to that in control cells. Genome-wide analysis revealed that PTEN loss lead to increase BRG1 intervals specifically localized at enhancers, but not distal promoter regions. We therefore reasoned ablation of BRG1 might impair enhancer configurations in PTEN-deficient cells.

2019-01-14 | GSE115615 | GEO

Expression profiles of Brg1-depleted acinar cells during ductal conversion

Project description:Brahma related gene 1 (BRG1), a catalytic ATPase subunit of SWI/SNF chromatin remodeling complexes, is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDA). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and IPMN-derived PDA from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia (PanIN) from acinar cells remains elusive. Here, we investigated the role of BRG1 in PanIN initiation and maintenance and its underlying mechanisms. Exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1f/f (KBC) mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independent of the presence of p53 mutation. We found that Sox9 expression was down-regulated in both Brg1-depleted acinar cell explants and BRG1-depleted ADMs/PanINs. Sox9 overexpression rescued this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1-deletion in established PanIN by using an inducible dual recombinase system resulted in regression of the lesions in mice. Finally, expression of BRG1 and SOX9 was also positively correlated in human PanIN-derived PDAs. In summary, BRG1 is critical for both initiation and maintenance of PanIN. Mechanistically, this is mediated through positive regulation of SOX9 expression. Thus, the BRG1/SOX9 axis is a potential target for the prevention of PanIN-derived PDA.

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Ablation of Pten and Smad4 leads to metastatic lung carcinoma in a murine model.

Project description:Lung cancer is the leading cause of cancer related death in both men and women in the United States. Recently, Smad4 was discovered to be common somatic alteration in human squamous cell lung cancer. Our goal was to delineate the role of Smad4 in lung cancer. We have shown for the first time that the ablation of Pten and Smad4 in the murine airway epithelium harbors a metastatic proximal adeno-squamous lung cancer. knockout group (PTENd/d and SMAD4d/d) and control group

2015-03-12 | E-GEOD-47116 | biostudies-arrayexpress

Compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells by ATAC-Seq

Project description:Compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells by ATAC-Seq

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Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

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Ablation of Pten and Smad4 leads to metastatic lung carcinoma in a murine model.

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Brg1 controls stemness and metastasis of pancreatic cancer through regulating hypoxia pathway

Project description:Brg1 is a subunit of SWI/SNF chromatin remodeling complex. To clarify the role of Brg1 for the progression and metastasis of pancreatic ductal adenocarcinoma (PDAC), we generated a PDAC mouse model with a dual recombinase system (Brg1 lox/lox; Pdx1-Flp; Kras FSF-G12D; Trp53 frt/frt; Rosa26 FSF-CreERT2) which enabled to ablate Brg1 in established PDAC with tamoxifen treatment. We established cancer cell lines derived from PDAC tumors developed in those mice and investigated the effect of Brg1 ablation on PDAC cell proliferation and metastasis. In order to determine the genes expression in Brg1-deleted mouse PDAC cells, we conducted a transcriptomic analysis using microarray using Brg1 wild type and Brg1-deleted mouse PDAC cells.

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SWI/SNF Chromatin Remodeling Factor BRG1 is Synthetic Required for PTEN-deficient Prostate Cancer

Project description:SWI/SNF Chromatin Remodeling Factor BRG1 is Synthetic Required for PTEN-deficient Prostate Cancer

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