The macrophage galactose-type C-type lectin 1 receptor plays a major role in mediating colitis-associated colorectal cancer malignancy.

Cancer-associated aberrant glycosylation can be detected by the macrophage galactose-type C-type lectin (MGL) receptor; however, whether this interaction enhances or deadens cancer development along with the associated immune response has not been well established. To determine the role of mouse MGL1 in colitis-associated colon cancer (CAC), azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced tumor development was compared between Mgl1 knockout (Mgl1) mice and their wild-type (WT) littermates. At 75 days post-CAC induction, colon tumor tissue contained more highly glycosylated proteins, representing potential ligands for the mMGL1 receptor, than did healthy colon tissue.