GCNT3 (glucosaminyl N-acetyl transferase 3) is a Golgi-localized glycosyltransferase that catalyzes core 2 and core 4 O-glycan branching in mucin-type biosynthesis 1. It mediates the synthesis of mucin β-1,6-N-acetylglucosaminides and possesses I-branching enzyme activity for poly-N-acetyllactosaminoglycan modifications 1. In cancer biology, GCNT3 exhibits context-dependent roles: elevated expression correlates with improved prognosis and chemotherapy sensitivity in ovarian cancer, whereas it associates with poor survival and immune suppression in pancreatic and lung cancers 1. In hepatocellular carcinoma, GCNT3 overexpression promotes tumor progression through MUC13-mediated activation of GSK3β/β-catenin signaling 2. GCNT3 knockdown in pancreatic cancer suppresses metastasis via downregulation of cell cycle genes and the β-catenin/MUC4 axis 3. In castration-resistant prostate cancer, elevated core 4-type O-glycans and GCNT3 expression facilitate epithelial-mesenchymal transition 4. Talniflumate, a GCNT3 inhibitor, reduces pancreatic cancer progression and enhances chemotherapy efficacy by impairing mucin-mediated immune suppression 5. GCNT3 serves as a potential prognostic biomarker and therapeutic target, though selective inhibition remains challenging given its essential roles in normal glycosylation.