Instead, OGT knockdown and OGT inhibitor treatment significantly increased Rab3A GTP-binding activity in Hep3B cells and OGT-overexpressed PLC/PRF/5 cells (p < 0.05) (Fig. 3f–i and Additional file 5: Figure S4a–c), indicating that elevated O-GlcNAcylation on Rab3A regulates the GTP-binding affinity of Rab3A in HCC cells. This evidence concerns the gene RAB3A and hepatocellular carcinoma.