B3GNT7 encodes a β-1,3-N-acetylglucosaminyltransferase that catalyzes transfer of GlcNAc to terminal galactose residues, functioning primarily in glycoprotein and proteoglycan biosynthesis 1. In intestinal epithelial cells, B3GNT7 regulates fucosylation of O-glycosylated glycoproteins, including mucins, through poly-N-acetyllactosamine chain synthesis 2. IL-22 signaling upregulates B3GNT7 expression to promote intestinal glycosylation and fucosylation of Lewis X antigens 2. B3GNT7 is critical for maintaining mucin barrier function; reduced expression correlates with increased colonic inflammation severity in ulcerative colitis patients and impaired inner mucus layer organization 3. In cancer biology, B3GNT7 acts as a tumor suppressor: suppressed expression in colorectal cancer cells (via promoter DNA methylation) promotes cell migration and liver metastasis by altering sialyl Lewis antigen display 4. Conversely, B3GNT7 overexpression in breast cancer correlates with poor prognosis and promotes cell proliferation, migration, and invasion through increased fucosylation 5. Oxytocin enhances B3GNT7-mediated fucosylation to alleviate colitis and colitis-associated colorectal tumorigenesis 1. DNA methylation of B3GNT7 serves as a prognostic marker for colorectal cancer survival outcomes 6. Thus, B3GNT7 exhibits context-dependent roles: protective in intestinal inflammation and colorectal metastasis, but protumorigenic in breast cancer.