The MicroRNAmiR-223constrains Colitis-associated tumorigenesis by limiting myeloid cell infiltration and Chemokine expression
Aberrant intestinal inflammation plays a critical role in the development of colitis-associated colorectal cancer (CAC), yet the mechanisms behind this progression are not clearly defined. While altered microRNA (miRNA) expression is observed in CAC, it is unclear how myeloid-specific microRNA's impact on the inflammatory process that underpins the continuum from Ulcerative colitis (UC) to tumorigenesis. Here we used the Azoxymethane-Dextran Sodium Sulfate (AOM-DSS) (10mg/kg) model of CAC on miR-223-/y and WT mice, with an overall aim of identifying differences in their expression profiles following AOM/DSS treatment. Overall design: To investigate the effects of miR-223 on the development of colitis associated colorectal cancer, we used miR-223-/y and C57BL/6J mice treated with azoxymethane(AOM)/dextran sodium sulfate(DSS) (10mg/kg). Total RNA was extracted from colonic tissue and gene expression analysis was performed on RNA-seq results.