GSE68306

• Patients with ulcerative colitis (UC) are at increased risk for colorectal cancer, although mechanisms underlying neoplastic transformation are poorly understood. 
• This study sought to evaluate the role of microRNAs in neoplasia development in this high-risk population.

• miR-31, miR-34a, miR-106b, and miR-193a-3p were significantly dysregulated in UC-neoplasia and adjacent tissue. 

• Significant down-regulation of miR-193a-3p was also seen in an independent cohort of UC-cancers. 
• Changes in methylation of miR-193a or expression of pri-miR-193a were not observed in UC-cancer. 
• Transfection of miR-193a-3p resulted in decreased proliferation, and identified IL17RD as a direct target of miR-193a-3p. I

• L17RD expression was increased in UC-cancers.
• miR-193a-3p treatment decreased growth and EGFR signaling of HCT116 cells in xenografts expressing both IL17RD with WT 3'UTR compared to cells expressing IL17RD with mutant 3'UTR.

• miR-193a-3p is down-regulated in UC-neoplasia, and its loss promotes carcinogenesis through up-regulation of IL17RD. 
• These findings provide novel insight into inflammation-driven CRC and could suggest new therapeutic targets in this high-risk population.

• A classification model has been built using Trainset (Control against Ulcerative colitis associated neoplastic tissues).
• The selected probe was:
  1. hsa-miR-135b

• The model has been tested using Testset.