The worldwide incidence rate for UC varies between 0.5–24.5 out of 100,000 persons for CD, between 0.1–16 and for IBD, the prevalence rate is as high as 396 per 100,000 persons worldwide ( Lakatos, 2006). This group includes Crohn disease (CD) and ulcerative colitis (UC). Inflammatory bowel diseases (IBD) are a group of autoimmune disorders that affect the gastrointestinal tract. Six of these miRNAs had a tumorigenic effect on the TP53 pathway the effect of three of which was studied using cell lines. Unique differentially expressed miRNAs were observed in CD-associated CRC progression. Additionally, cyclin G, a cell-cycle regulator miR-122 target was down-regulated in both cell lines ( p<0.05). Using two human colon cancer cell lines (HT-29 and HCT-116), E2F1, an upstream regulator of TP53, was down-regulated in both cell lines transfected with let-7e ( p<0.05) as well as in HCT-116 cells transfected with miR-17 ( p<0.05). Six differentially expressed miRNAs affected the TP53 pathway ( miR-122, miR-214, miR-372, miR-15b, let-7e, miR-17) ( p<0.001). In our CD patients, six miRNAs were up-regulated from non-neoplastic tissue to dysplasia, but down-regulated from dysplasia to cancer ( miR-122, miR-181a, miR-146b-5p, let-7e, miR-17, miR-143) ( p<0.001). In addition, we identify and examine the role of dysregulated miRNAs in the TP53 pathway. In this study, we report differential miRNA expression in IBD patients with associated CRC, from non-neoplastic tissue to dysplasia and eventually cancer. MicroRNAs (miRNAs) are small non-protein-coding RNAs that play important roles in CRC oncogenesis. There is a compelling need to enhance the accuracy of cancer screening of IBD patients. One of the most serious complications faced by inflammatory bowel disease (IBD) is the potential development of colorectal cancer (CRC).
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