Project description:Analysis of expression changes between colon tumors (Duke's stage II) and matching colon mucosa tissues using Affymetrix GeneChip® Human Gene 2.0 ST arrays.
Project description:Analysis of expression changes between colon tumors (Duke's stage II) and matching colon mucosa tissues using Affymetrix GeneChip® Human Gene 2.0 ST arrays. All experiments were performed simultaneously for matching tissue samples.
Project description:We used NimbleGen human CpG/promoter microarrays for profiling epigenetic changes (DNA methylation, H3K27me3 and H3K4me3 marks) in colon tumors (Duke's stage II) and matching mucosa samples from patients.
Project description:Comparing to matched normal mucosa, WTX was lost in most of human colorectal cancers (Zhang et al., 2016). We analyzed the microRNA expression profiling among WTX low human colorectal cancer tissues and matched adjacent WTX high normal colorectal mucosa. The aimed to identify the unique signature of miRNAs which related to WTX loss in human colorectal cancers.
Project description:Comparing to matched normal mucosa, WTX was lost in most of human gastric cancers (Zhang et al., 2016). We analyzed the microRNA expression profiling among WTX low human colorectal cancer tissues and matched adjacent WTX high normal colorectal mucosa. The aimed to identify the unique signature of miRNAs which related to WTX loss in human colorectal cancers.
Project description:We used NimbleGen human CpG/promoter microarrays for profiling epigenetic changes (DNA methylation, H3K27me3 and H3K4me3 marks) in colon tumors (Duke's stage II) and matching mucosa samples from patients. Analysis of DNA methylation was done by using the methylated CpG island recovery assay (MIRA) technique with further hybridization versus input on NimbleGen human CpG/promoter microarrays. For profiling of H3K27me3 and H3K4me3 marks, we performed chromatin immunoprecipitation with H3K27me3 (#07-449, Millipore) and H3K4me3 (#39159, Active Motif) antibodies and further hybridized versus input on NimbleGen human CpG/promoter microarrays. All experiments were performed simultaneously for matching tissue samples.
Project description:DNA methylation is an epigenetic mark that is altered in cancer and aging tissues. The effects of extrinsic factors on DNA methylation remain incompletely understood. Microbial dysbiosis is a hallmark of colorectal cancer, and infections have been linked to aberrant DNA methylation in cancers of the GI tract. To determine the microbiota’s impact on DNA methylation, we studied the DNA methylation of colorectal mucosa in germ-free (GF, no microbiome) and specific pathogen free (SPF, controlled microbiome) mice, as well as in interleukin 10 KO mice (Il10-/-) which are prone to inflammation and tumorigenesis in the presence of a microbiome. We compared DNA methylation changes to those seen in aging, and after exposure to the colon carcinogen azoxymethane (AOM). DNA methylation changes associated with aging were accelerated in the Il10-/- /SPF mice. By contrast, AOM induced profound hypomethylation that was distinct from the effects of aging or of the microbiome. CpG sites modified by the microbiome were over-represented among DNA methylation changes in colorectal cancer. Thus, the microbiome affects the DNA methylome of colorectal mucosa in patterns reminiscent of what is observed in colorectal cancer.
