GCNT2 encodes a β-1,6-N-acetylglucosaminyltransferase that determines expression of the blood group I antigen on erythrocytes by converting linear i-antigen to I-branched glycans 1. Beyond its canonical blood group function, GCNT2 plays a context-dependent role in human disease. In cancer biology, GCNT2 exhibits dual roles depending on cancer type. In melanoma, GCNT2 loss promotes tumor growth and survival by reducing I-branched glycan modifications on insulin-like growth factor receptors and integrins, thereby dampening critical signaling pathways 2. Conversely, GCNT2 overexpression drives progression in esophageal squamous cell carcinoma and prostate cancer by inducing epithelial-mesenchymal transition (EMT) and enhancing migration/invasion through α5β1 integrin signaling 34. In acute myeloid leukemia, hypomethylation of GCNT2 isoform A associates with high-risk disease and poor survival 5. Mechanistically, GCNT2 is regulated by miR-199a/b-5p during EMT in colon cancer 1, and its expression is controlled by DNA methylation in AML 5. In bone metabolism, GCNT2 suppression promotes osteoblast differentiation via PI3K/AKT/mTOR pathway activation, suggesting therapeutic potential in osteoporosis 6. GCNT2 represents an emerging biomarker and therapeutic target across multiple malignancies 7.
No tissue expression data available for this gene.