Table 1.
Changes in glycosylation associated with hepatocellular carcinoma phenotype.
| Glycan modification | Proposed major function | Reference |
|---|---|---|
| Increased β-1,6-GlcNAc branching on N-glycans | Decreased cell adhesion to fibronectin | (110) |
| Increased sialylated GlcNAc branching on N-glycans | Decreased cell–cell interaction, enhanced motility and invasiveness | (110) |
| Increased fucosylation of core and outer-arm | Decreased cell polarity and altered adhesive properties | (99–102) |
| Increased fucosylation and sialylation of β chain on haptoglobin | Altered adhesive properties | (83) |
| Increased expression of sLe structures | Enhanced tumor cell adhesion during metastasis | (25, 47) |
| Increased expression of high-mannose structures | Enhanced proliferation, adhesion, and metastasis | (25, 29, 95) |
| Increased fucosylated, sialylated, and complex N-glycans | Increase activity of the epidermal growth factor receptor (EGF-R), decreased cell–cell interaction, enhanced motility and invasiveness | (27, 103, 105–107) |
| Increased of bi-sialylated O-glycopeptide of hemopexin | Altered adhesive properties | (107) |
| Increased expression of multiply fucosylated Ley in haptoglobin | Enhanced tumor cell adhesion during metastasis | (108) |
| Increased of core-α-1,6-fucosylated triantennary glycan | Enhanced cell migration | (109) |
| Increased of α-1,3-fucosylated branching on triantennary glycan | Decreased cell polarity and altered adhesive properties | (104) |