Project description:To find out which miRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed miRNA microarray as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The miRNA microarray experiments were performed together.
Project description:To investigate the biological function Trim21 in the colon cancer, we compared the gene expression profiles of colon tumor tissues from Trim21 +/+ and Trim21 -/- mice treated with the carcinogen azoxymethane (AOM) and the proinflammatory agent dextran sulfate sodium (DSS).
Project description:To find out which mRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The whole genome microarray expression profiling experiments were performed together.
Project description:To understand how specifically intestinal ERβ impacts the transcriptome during colitis and tumor develpment, sequencing was perfromed on colon epithelium from AOM/DSS or vehicle treated mice, and tumors from treated mice.
Project description:mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- mRNA expression data
Project description:mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray
Project description:The objective of the study was to evalute the changes in gene expression associated to UCP2 invalidation in colon tumors from AOM/DSS-treated mice We used microarrays (Mouse Gene 2.0) to investigate gene expression in Ucp2+/+ and Ucp2-/- colon tumors
Project description:This study identifies a novel mechanism linking IL-17A with colon tissue repair and tumor development. Abrogation of IL-17A signaling mice attenuated tissue repair of DSS-induced damage in colon epithelium and markedly reduced tumor development in AOM/DSS model of colitis-associated cancer. The goal of these studies is to identify genes associated with IL-17RC deficiency during AOM-DSS induced tumorigenesis
Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of mRNA expression profile for colon tissues from wildtype and CARD9 knockout mice treated with AOM/DSS
