GSE178144
AOM/DSS colorectal cancer mouse epigenetic landscape in the progression of colites to tumor [ChIP-seq]
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. Overall design: ChIP-seq samples of 5 different marks (H3K27ac, H3K4me1, H3K4me3, H3K27me3, H3K9me3) across 5 time point (week-0, week-2, week4, week-7, week-10)