Ontology highlight
ABSTRACT:
PROVIDER: PRJNA910503 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22587163_1.fastq.gz | Fastqsanger.gz | |||
| SRR22587163_2.fastq.gz | Fastqsanger.gz | |||
| SRR22587164_1.fastq.gz | Fastqsanger.gz | |||
| SRR22587164_2.fastq.gz | Fastqsanger.gz | |||
| SRR22587165_1.fastq.gz | Fastqsanger.gz |
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Project description:Ulcerative Colitis is an autoimmune inflammatory bowel disease that causes chronic inflammation in the colon and the rectum. Althoung extensively researched, the underlying molecular mechanisms of Ulcerative Colitis remain elusive. Especially, there is a lack of understanding about regulatory non-coding miRNA expression during Ulcerative Colitis. Therefore, we performed high-throughput miRNA profiling of colon tissue biopsies from XX patients with active Ulcerative Colitis, XX patients with quiescent Ulcerative Colitis and XX Symptomatic Control individuals.
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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.
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Project description:Legumain is a cysteine protease broadly associated with inflammation. It has recently been reported to cleave and activate protease-activated receptor 2 to provoke pain associated with oral cancer. Outside of gastric and colon cancer, little has been reported on the roles of legumain within the gastrointestinal tract. Using a legumain-selective activity-based probe, LE28, we report that legumain is activated within colonocytes and macrophages of the murine colon, and that it is upregulated in models of acute experimental colitis induced by DSS and TNBS. We demonstrated that loss of legumain activity in colonocytes, either through pharmacological inhibition or gene deletion, had no impact on epithelial permeability in vitro. Moreover, legumain inhibition or deletion had no obvious impacts on symptoms or histological features associated with DSS-induced colitis, suggesting its proteolytic activity is dispensable for colitis initiation. To gain insight into potential functions of legumain within the colon, we performed FAIMS-facilitated quantitative proteomics and N-terminomics analyses on naïve and inflamed colon tissue from wild-type and legumain-deficient mice. We identified 16 altered cleavage sites with an asparaginyl endopeptidase signature that may be direct substrates of legumain and a further 16 cleavage sites that may be indirectly mediated by legumain. We also analyzed changes in protein abundance and proteolytic events broadly associated with colitis in the gut, which permitted comparison to recent analyses on mucosal biopsies from patients with inflammatory bowel disease. Collectively, these results shed light on potential functions of legumain and highlight its potential roles in the transition from inflammation to colorectal cancer.
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Project description:Ulcerative Colitis is an autoimmune inflammatory bowel disease that causes chronic inflammation in the colon and the rectum. Althoung extensively researched, the underlying molecular mechanisms of Ulcerative Colitis remain elusive. Especially, there is a lack of understanding about regulatory non-coding miRNA expression during Ulcerative Colitis in a cell type-specific context. Therefore, we performed high-throughput miRNA profiling of Fluorescence Activated Cell Sorting (FACS)-enriched CD66a+ and CD44+ colonic epithelial cell populations from colon tissue biopsies of 16 patients with active Ulcerative Colitis, 15 patients with quiescent Ulcerative Colitis and 17 Symptomatic Control individuals.
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