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

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

PROVIDER: PRJNA475577 | ENA |

REPOSITORIES: ENA

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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

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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RNA-seq of PTEN knockdown in GL261 cells

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Genome-wide occupancy of chromatin remodeller SMARCAL1 and BRG1 in human cells

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2019-09-12 | GSE137250 | GEO

Comparison of gene expression in control and BRG1-knockdown H358 cell lines

Project description:Transcription was assessed in the human H358 NSCLC cell line after knockdown of BRG1, one of the mutually exclusive subunits of the SWI/SNF chromatin remodeling complex, by 2 different shRNAs. One biolgical replicate of each treatment; 4 technical replicates of each treatment.

2014-09-23 | E-GEOD-58542 | biostudies-arrayexpress

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Project description:Non-small cell lung cancers (NSCLCs) harbor thousands of passenger events that hide genetic drivers. Even highly recurrent events in NSCLC, such as mutations in PTEN, EGFR, KRAS, and ALK, are only detected in, at most, 30% of patients. Thus, many unidentified low-penetrant events are causing a significant portion of lung cancers. To detect low-penetrance drivers of NSCLC a forward genetic screen was performed in mice using the Sleeping Beauty (SB) DNA transposon as a random mutagen to generate lung tumors in a Pten deficient background. SB mutations coupled with Pten deficiency were sufficient to produce lung tumors in 29% of mice. Pten deficiency alone, without SB mutations, resulted in lung tumors in 11% of mice, while the rate in control mice was ~3%. In addition, thyroid cancer and other carcinomas as well as the presence of bronchiolar and alveolar epithelialization in mice deficient for Pten were also identified. Analysis of common transposon insertion sites identified 76 candidate cancer driver genes. These genes are frequently dysregulated in human lung cancers and implicate several signaling pathways. Cullin3 (Cul3), a member of an ubiquitin ligase complex that plays a role in the oxidative stress response pathway, was identified in the screen and evidence demonstrates that Cul3 functions as a tumor suppressor HumanHT-12 v4 Expression BeadChip Kit for human A549 lung adenocarcinoma cells with CUL3, PTEN, CUL3 and PTEN or no knockdown. A549 cells were stably transfected under Puromycin or Hygromycin selection to knockdown PTEN (SA Biosystems) or CUL3 (Open Biosystems) shRNAs. RNA was extracted in triplicate from each condition and used for microarray

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RNA-seq of PTEN knockdown in GL261 cells

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