Gene expression analysis in Tyk2 deficient AOM/DSS colorectal tumors in mice
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PROVIDER: PRJNA837873 | ENA |
REPOSITORIES: ENA
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Project description:The goal of this study was to determine differences in gene expression profiles in colonic tumors of AOM/DSS treated mice with a total (Tyk2KO) or conditional deletion of Tyk2 in the intestinal epithelium (Tyk2DIEC).
2022-07-01 | GSE202954 | GEO
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.
2013-05-10 | E-GEOD-44983 | biostudies-arrayexpress
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.
2013-05-10 | E-GEOD-44904 | biostudies-arrayexpress
Project description:The tumor microenvironment plays a key role in the pathogenesis of colorectal tumors and contains various cell types including epithelial, immune, and mesenchymal cells. Characterization of the interactions between these cell types is necessary for revealing the complex nature of tumors. In this study, we used single-cell RNA-seq (scRNA-seq) to compare the tumor microenvironments between a mouse model of sporadic colorectal adenoma (Lrig1CreERT2/+;Apc2lox14/+) and a mouse model of inflammation-driven colorectal cancer induced by azoxymethane and dextran sodium sulfate (AOM/DSS). While both models develop tumors in the distal colon, we found that the two tumor types have distinct microenvironments. AOM/DSS tumors have an increased abundance of two populations of cancer-associated fibroblasts (CAFs) compared with APC tumors, and we revealed their divergent spatial association with tumor cells using multiplex immunofluorescence (MxIF) imaging. We also identified a unique squamous cell population in AOM/DSS tumors, whose origins were distinct from anal squamous epithelial cells. These cells were in higher proportions upon administration of a chemotherapy regimen of 5-Fluorouracil/Irinotecan. We used computational inference algorithms to predict cell-cell communication mediated by ligand-receptor interactions and downstream pathway activation, and identified potential mechanistic connections between CAFs and tumor cells, as well as CAFs and squamous epithelial cells. This study provides important preclinical insight into the microenvironment of two distinct models of colorectal tumors and reveals unique roles for CAFs and squamous epithelial cells in the AOM/DSS model of inflammation-driven cancer. This series comprises the drug treatment set as well as the fibroblast enrichment set.
2022-04-27 | GSE199999 | GEO
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.
2013-05-10 | GSE44983 | GEO
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.
2013-05-10 | GSE44904 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to analysis NGS-derived transcriptome profiling (RNA-seq) in DSS induced chronic inflammation, AOM/DSS induced colitis-associated colorectal tumorigenesis and organoids isolation from colitis-associated colorectal tumorigenesis Methods: DSS, AOM/DSS and organoids mRNA profiles of wild-type (WT) and RING Finger 3 (RNF138−/−) mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500. The sequence reads were trimmed for low-quality sequence, then mapped to mm10 whole genome using STAR v2.6.1d Results: Using an optimized data analysis workflow, the padj <0.05 and fold change >2 were refered as differential expression. There are 987, 2649 and 2373 differential genes were found in RNF138-/- compared with Wild Type in DSS, AOM/DSS and organoids, respectively Conclusions: Our study revealed NFκB pathway is the main activation pathway regulated by RNF138 loss
2022-04-30 | GSE144051 | GEO
Project description:Purpose : The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) of colon samples of intestinal epithelial cell specific Axin1 Knockout mice and WT controls that were submitted to DSS-induced colitis and AOM/DSS-induced colorectal carcinogenesis. Methods : DSS-induced colitis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice by giving 3% DSS dissolved in drinking water for 7 days and subsequently placed on regular water for recovery before sacrifice at Day 7 and D13. Methods : AOM/DSS-induced colorectal tumorigenesis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice that were sacrificed at day 100 post-AOM injection to collect colorectal tumors. Methods : Colonic mRNA profiles of WT and Axin1KOΔIEC mice were generated by deep sequencing using Illumina NextSeq 500 instrument (150base-lengths read V2 chemistry in a paired-end mode)
2022-02-09 | GSE196220 | GEO
Project description:Azoxymethane (AOM) and dextran sulfate sodium (DSS) mice, as a classic model for the study of colorectal cancer, can completely simulate the inflammatory cancer transformation in the development of colorectal cancer.Although people have been trying to reveal the key mechanism of colorectal cancer transformation. But the current understanding of it is still not enough. In this study, we injected mice with AOM and then periodically treated them with DSS. The mice were made to develop tumors in the colon finally. In this process, we sampled the intestinal tissues of the mice at different time points, respectively, at the 0th week, 2nd week, 4th week, 7th week and 10th week after AOM injection. to describe the gene exprression profile across all time point, we get the RNA-seq data for all samples.
2022-06-14 | GSE178145 | GEO
Project description:Azoxymethane (AOM) and dextran sulfate sodium (DSS) mice, as a classic model for the study of colorectal cancer, can completely simulate the inflammatory cancer transformation in the development of colorectal cancer.Although people have been trying to reveal the key mechanism of colorectal cancer transformation. But the current understanding of it is still not enough. In this study, we injected mice with AOM and then periodically treated them with DSS. The mice were made to develop tumors in the colon finally. In this process, we sampled the intestinal tissues of the mice at different time points, respectively, at the 0th week, 2nd week, 4th week, 7th week and 10th week after AOM injection. In order to fully describe the epigenetic pattern of colorectal cancer in AOM/DSS mice, especially the dynamic changes in the process of inflammatory cancer transformation. we generated the histone modification profile of 5 markers, including H3K27Ac (active enhancer), H3K4me1 (enhancer), H3K4me3 (promoter), H3K9me3 (heterochromatin) and H3K27me3 (multicomb suppression) across 5 time points (week-0, week-2, week-4, week-7, week-10). Genome-wide epigenetic analysis found that during the tumorigenesis process, enhancer chromatin state region increased. And functionally related to apoptosis and mitochondrial function. When detecting the dynamic changes of the signal intensity of H3K27ac, it was found that the enhanced enhancer signal-related genes were enriched in the inflammatory factor NFKB signaling pathway. It shows that in the process of inflammatory cancer transformation, H3K27ac are involved in inflammation and cell apoptosis, and play an important role in inflammatory cancer transformation.
2022-06-14 | GSE178144 | GEO