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AOM/DSS colorectal cancer mouse epigenetic landscape in the progression of colites to tumor [ChIP-seq]

ABSTRACT: AOM/DSS colorectal cancer mouse epigenetic landscape in the progression of colites to tumor [ChIP-seq]

PROVIDER: PRJNA737464 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14807900_1.fastq.gz	Fastqsanger.gz
	SRR14807900_2.fastq.gz	Fastqsanger.gz
	SRR14807901_1.fastq.gz	Fastqsanger.gz
	SRR14807901_2.fastq.gz	Fastqsanger.gz
	SRR14807902_1.fastq.gz	Fastqsanger.gz

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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: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.

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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: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

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

2013-05-10 | GSE44983 | GEO

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

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AOM/DSS colorectal cancer mouse epigenetic landscape in the progression of colites to tumor [ChIP-seq]

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.

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Project description:To unbiasedly characterize the spatial transcriptomics landscape of murine colorectal cancer initiation and progression, we performed a time-series spatial transcriptional analysis of total colonic tissue during the course of azoxymethane (AOM)-dextran sodium sulfate (DSS) induced colorectal cancer from mice receiving standard (chow) diet. Additionally, to understand the role of LXR activation during AOM-DSS tumorigenesis, we also collected colonic tissues from mice fed with GW3965 diet.

2024-07-19 | GSE227598 | GEO

AOM/DSS colorectal cancer mouse transcriptome profile across 5 time point in the progression of colites to tumor [RNA-seq]

2022-06-14 | GSE178145 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and RNF138-/- mice colorectal transcriptomes in DSS, AOM/DSS and organoids samples

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

Time-series transcriptomic analysis of murine colon undergoing AOM-DSS tumorigenesis with and without LXR activation

Project description:To unbiasedly characterize the differentially expressed genes and pathways during colorectal cancer initiation and progression, we performed a time-series transcriptional analysis of total colonic tissue during the course of azoxymethane (AOM)-dextran sodium sulfate (DSS) induced colorectal cancer from mice receiving standard (chow) diet. Additionally, to understand the role of LXR activation during AOM-DSS tumorigenesis, we also collected colonic tissues from mice fed with GW3965 diet.

2024-07-19 | GSE180078 | GEO

AOM/DSS tumors 5FU+Irinotecan treatment

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.

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