| Objective: We transfected combinant plasmid of GOLPH2 WT and GOLPH2 DM into Hep G2 cells to study the effect of GOLPH2 glycosylation modification on cell growth, cycle cycle, inflammatory pathway and cholesterol metabolism, in order to demonstrate the role of GOLPH2 glycosylation modification in hepatocarcinogenesis.Methods: We constructed eukaryotic expression vector of GOLPH2 without glycosylation modification and named it pc DNA3-Flag-GOLPH2(DM). We transfected GOLPH2 WT and GOLPH2 DM into Hep G2 cells and tested cell proliferation by cell growth assay, cell cycle by cell cycle arrest assay, NF-κB activation by NF-κB dual-luciferase reporter assay, inflammasome activation and lipid raft accumulation by immunofluorescence.Results: The results show that GOLPH2 makes Hep G2 cell grow fast, but GOLPH2 DM slows this process. The dual-luciferase reporter assay indicates that GOLPH2 activates the transcriptional activity of NF-κB in Hep G2 cells, yet GOLPH2 DM losts this function. Immunofluorescence tests find GOLPH2 prompts the accumulation of inflammasome and lipid raft in Hep G2 cells, however, GOLPH2 DM has no such effect.Conclusion: GOLPH2 glycosylation modification promotes the growth of hepatocellular carcinoma cells; GOLPH2 glycosylation modification may be involved in activating inflammatory signaling pathway; GOLPH2 glycosylation modification may be involved in regulating cholesterol metabolism; GOLPH2 glycosylation modification for its function is indispensable. |