Function of Epithelium BRG1 in colitis and CAC II
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ABSTRACT:
PROVIDER: PRJNA496292 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8052150_1.fastq.gz | Fastqsanger.gz | |||
| SRR8052150_2.fastq.gz | Fastqsanger.gz | |||
| SRR8052147_1.fastq.gz | Fastqsanger.gz | |||
| SRR8052147_2.fastq.gz | Fastqsanger.gz | |||
| SRR8052148_1.fastq.gz | Fastqsanger.gz |
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Project description:Function of Epithelium BRG1 in colitis and CAC
| PRJNA439218 | ENA
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
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
Project description:Function of BRG1 in colitis and colitis-associated-cancer
| PRJNA439385 | ENA
Project description:To uncover molecular mechanisms specifically involved in the pathogenesis of colitis-associated colon cancer (CAC), we studied tumorigenesis in experimental models of CAC and sporadic CRC that mimic characteristics of human CRC. Using comparative whole genome expression profiling, we observed differential expression of epiregulin (Ereg) in mouse models of colitis-associated, but not sporadic colorectal cancer. Similarly, highly significant upregulation of Ereg expression was found in cohorts of patients with colitis-associated cancer in inflammatory bowel disease but not in sporadic colorectal cancer. Furthermore, tumor-associated fibroblasts were identified as major source of Ereg in colitis-associated neoplasias. Functional studies showed that Ereg-deficient mice, although more prone to colitis, are strongly protected from colitis-associated tumors, and data from serial endoscopic studies revealed that Ereg promotes growth rather than initiation of tumors. 4 samples of individual distal colitis-associated tumors (CAC) from 4 mice, 2 samples of tumor-free distal colon epithelium with a pool of 5 mice per sample (CAC contr), 5 samples of individual Apcmin/+ tumors from the distal colorectum of 5 mice (sporCRC) and 3 samples of tumor-free distal colon epithelium (pool of 4 mice per sample) (sporCRC contr). Colitis-associated tumorigenesis was performed by intraperitoneal injection of Azoxymethane (10mg/kg) (Sigma) into C57BL/6J wildtype mice followed by 3 cycles of Dextran Sodium Sulfate (DSS) in drinking water. Each DSS-cycle was composed of DSS (2.5% (w/v) (MP Biomedicals) in drinking water for 7 days, followed by a recovery phase with regular drinking water for 14 days. Sporadic tumors were from C57BL/6J-ApcMin/+/J mice. All tumors were obtained from the from the lower 6th of the large intestine and they had the same size covering between ¼ and up to ½ of the colonic circumferenc as evaluated by mini-endoscopy.
2013-04-01 | E-GEOD-43338 | biostudies-arrayexpress
Project description:Brg1 has been reported to act as a trans-activator for the Wnt pathway by interacting with beta-catenin. Given this interaction and the crucial role Wnt signalling plays in the intestinal homeostasis, we aimed to investigate the effect of Brg1 loss on gene expression in normal and Wnt activated small intestinal epithelium. We used VillinCreERT2 Cre recombinase and loxP targeted allels of Brg1 and Apc to generate 4 cohorts of conditional knock-out mice: Cre-negative controls (n=4), Brg1 deficient (n=4), Apc deficient (n=3) and double Brg1-Apc deficient (n=4). All mice were induced by 4x80mg/kg daily injections of Tamoxifen. Epithelium enriched (gut scrapes) samples of small intestine (jejunum) were collected at day 4 post induction. Loss of Brg1 expression in the small intestinal epithelium at this time point was confirmed by immunohistochemistry.
2013-08-07 | E-GEOD-46129 | biostudies-arrayexpress
Project description:Aberrant epithelial differentiation and regeneration contribute to colon pathologies, including inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Myeloid translocation gene 16 (MTG16, also known as CBFA2T3) is a transcriptional corepressor expressed in the colonic epithelium. MTG16 deficiency in mice exacerbates colitis and increases tumor burden in CAC, though the underlying mechanisms remain unclear. Here, we identified MTG16 as a central mediator of epithelial differentiation, promoting goblet and restraining enteroendocrine cell development in homeostasis and enabling regeneration following dextran sulfate sodium–induced (DSS-induced) colitis. Transcriptomic analyses implicated increased Ephrussi box–binding transcription factor (E protein) activity in MTG16-deficient colon crypts. Using a mouse model homozygous for a point mutation that attenuates MTG16:E protein interactions (Mtg16P209T), we showed that MTG16 exerts control over colonic epithelial differentiation and regeneration by repressing E protein–mediated transcription. Mimicking murine colitis, MTG16 expression was increased in biopsies from patients with active IBD compared with unaffected controls. Finally, uncoupling MTG16:E protein interactions partially phenocopied the enhanced tumorigenicity of Mtg16-null colon in the azoxymethane (AOM) /DSS-induced model of CAC, indicating that MTG16 protects from tumorigenesis through additional mechanisms. Collectively, our results demonstrate that MTG16, via its repression of E protein targets, is a key regulator of cell fate decisions during colon homeostasis, colitis, and cancer.
2022-05-01 | GSE201768 | GEO
Project description:Aberrant intestinal inflammation plays a critical role in the development of colitis-associated colorectal cancer (CAC), yet the mechanisms behind this progression are not clearly defined. While altered microRNA (miRNA) expression is observed in CAC, it is unclear how myeloid-specific microRNA’s impact on the inflammatory process that underpins the continuum from Ulcerative colitis (UC) to tumorigenesis. Here we used the Azoxymethane-Dextran Sodium Sulfate (AOM-DSS) (10mg/kg) model of CAC on miR-223-/y and WT mice, with an overall aim of identifying differences in their expression profiles following AOM/DSS treatment.
2024-10-01 | GSE245724 | GEO
Project description:Although ageing is usually regarded as a high risk of cancer, the relationship between ageing stromal microenvironment and spontaneous cancer initiation is poorly understood. In murine models of DSS-induced colitis and AOM/DSS-induced colitis-associated cancer (CAC), we found ageing significantly inhibit both intestinal wound healing and simultaneous CAC initiation. In young mice, through conditional lineage tracing, a novel and important source of fibroblasts transformed from intestinal smooth muscle cells (ISMCs) was identified during intestinal wound healing, which existed persistently in CAC. We further found that activation of YAP/TAZ in ISMCs is required for their transformation into fibroblasts. However, in ageing intestinal microenvironment, the failure of YAP/TAZ activation in ISMCs led to reduced fibroblast numbers, orchestrating the inhibition of wound healing and simultaneous inhibition of CAC initiation. Collectively, our work revealed an important role of ageing stromal microenvironment in intestinal wound healing and CAC development. Meanwhile, our work also discovered an important source of fibroblasts involved in colitis and CAC.
2023-08-21 | GSE143693 | GEO
Project description:To uncover molecular mechanisms specifically involved in the pathogenesis of colitis-associated colon cancer (CAC), we studied tumorigenesis in experimental models of CAC and sporadic CRC that mimic characteristics of human CRC. Using comparative whole genome expression profiling, we observed differential expression of epiregulin (Ereg) in mouse models of colitis-associated, but not sporadic colorectal cancer. Similarly, highly significant upregulation of Ereg expression was found in cohorts of patients with colitis-associated cancer in inflammatory bowel disease but not in sporadic colorectal cancer. Furthermore, tumor-associated fibroblasts were identified as major source of Ereg in colitis-associated neoplasias. Functional studies showed that Ereg-deficient mice, although more prone to colitis, are strongly protected from colitis-associated tumors, and data from serial endoscopic studies revealed that Ereg promotes growth rather than initiation of tumors.
2013-04-01 | GSE43338 | GEO