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Function of BRG1 in colitis and colitis-associated-cancer

ABSTRACT: Function of BRG1 in colitis and colitis-associated-cancer

PROVIDER: PRJNA439385 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6869135.fastq.gz	Fastqsanger.gz
	SRR6869136.fastq.gz	Fastqsanger.gz
	SRR6873677.fastq.gz	Fastqsanger.gz
	SRR6873678.fastq.gz	Fastqsanger.gz
	SRR8052150_1.fastq.gz	Fastqsanger.gz

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Function of Epithelium BRG1 in colitis and CAC

Project description:Here we show that epithelial BRG1, the catalytic subunit of SWI/SNF complex is critical for colitis and colitis-associated-cancer. Depletion of BRG1 in colonrectal epithelial cells make mice develop Spontaneous colitis. To dissect underlying mechanism, we conducted gene expression profile analysis (RNA-Seq) by using primary colonrectal epithelial cells isolated from BRG1CTRL and BRG1IEC-KO(Tamoxifen induced BRG1 knock-out) mice to gain molecular insights into the affected biological processes. To this end, colorectal epithelial cells were isolated after 14 days of tamoxifen treatment, on which day BRG1-depleted mice showed little morphological defects in colon in comparison with control littermates. IECs were isolated by EDTA isolation buffer. Each sample contains pooled mRNA from 3 mice, and was subjected to Hiseq RNA-Seq, performed by BGI Tech Solutions Co., Ltd.

2019-03-01 | GSE112069 | GEO

Function of Epithelium BRG1 in colitis and CAC II

Project description:Here we show that epithelial BRG1, the catalytic subunit of SWI/SNF complex is critical for colitis and colitis-associated-cancer. Depletion of BRG1 in colonrectal epithelial cells make mice develop Spontaneous colitis. To dissect underlying mechanism, we conducted gene expression profile analysis (RNA-Seq) by using primary colonrectal epithelial cells isolated from BRG1CTRL and BRG1IEC-KO(Tamoxifen induced BRG1 knock-out) mice to gain molecular insights into the affected biological processes. To this end, colorectal epithelial cells were isolated after 7 days of tamoxifen treatment, on which day BRG1-depleted mice showed little morphological defects in colon in comparison with control littermates. IECs were isolated by EDTA isolation buffer. Each sample contains pooled mRNA from 3 mice, and was subjected to Hiseq RNA-Seq, performed by Guangzhou RiboBio Co., Ltd. (Guangzhou, China)using IlluminaHiSeq 3000 platform.

2019-03-01 | GSE121206 | GEO

Function of Epithelium BRG1 in colitis and CAC

Project description:Function of Epithelium BRG1 in colitis and CAC

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Function of Epithelium BRG1 in colitis and CAC II

Project description:Function of Epithelium BRG1 in colitis and CAC II

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Genome-wide assay of BRG1 regulated genes in inflamed colon epithelial cells

Project description:Here we focus on the function of BRG1 in colitis and colitis-associated-cancer, in the aim of finding the direct target genes of BRG1 which may response for the phenotype we observed in BRG1 conditional knock-out mice, ChIP-Seq assay is used. The cells used for ChIP-Seq is colon epithelial cells which isolated from DSS treated mice.

2019-03-01 | GSE112127 | GEO

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

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

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BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer

Project description:Deregulation of the chromatin remodeller BRG1 contributes to a wide range of malignancies. In prostate cancer BRG1 is over expressed, however, the underlying function and cellular consequences of this are still being uncovered. Here, we have investigated the role of BRG1 in transcription regulation in prostate cancer. We found that BRG1 is over expressed in both the TCGA prostate cancer cohort as well as a panel of prostate cancer and transformed prostate cell lines. We then utilised a temporal model of BRG1 depletion followed by mRNA-seq to examine changes in gene expression. Surprisingly, we detected a modest overall effect, however, a number of genes associated with proliferation and cell cycle progression were down regulated. We find these genes were in part, co-regulated by AR and FOXA1. Corresponding cell cycle analysis conferred G1 arrest, and altered nuclei morphology with depletion of BRG1. This data provides mechanistic insight into the function of BRG1 in prostate cancer.

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Cardamonin repel colitis and its associated colorectal cancer

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Function of BRG1 in colitis and colitis-associated-cancer

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

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Differential role of HNF4α isoforms in colitis and colitis-associated colon cancer

Project description:Hepatocyte nuclear factor 4alpha (HNF4α) is a nuclear receptor with an emerging role in the gut. While HNF4α has been implicated in colitis and colon cancer in humans, deciphering its functional role is complicated by the existence of two promoters (P1 and P2) in theHNF4A gene that drive the expression of multiple isoforms in the adult intestine. In this study we investigate the roles of P1- and P2-driven HNF4α under conditions of homeostasis, colitis and colitis-associated colon cancer (CAC). P1- and P2-HNF4α are differentially expressed in the differentiated and proliferative compartments of the normal colonic crypt, respectively. Expression profiling of untreated exon swap mice suggests distinct functions of the isoforms that were corroborated in migration and ion transport assays.

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