Conclusion
HS6ST2 promotes GC progression through the modulation of the TGF-β/smad2/3 pathway.
Methods
HS6ST2 expression in GC and adjacent normal gastric mucosa was first detected via immunohistochemical (IHC) staining. The correlation between the expression level of HS6ST2 and clinicopathological parameters were observed. The protein expression of HS6ST2 in AGS, MKN45 and GES-1 cells was examined using Western blotting. The function of HS6ST2 in GC cells was explored via CCK-8, wound healing and Transwell assays. To elucidate the underlying molecular mechanisms, we detected whether HS6ST2 modulated the TGF-β/smad2/3 signaling pathway. Finally, we investigated the role of HS6ST2 in tumor growth in a nude mouse model.
Objective
To investigate the role of heparan sulfate 6-O-sulfotransferase 2 (HS6ST2) in gastric cancer (GC).
Results
The expression level of HS6ST2 in GC tissues was significantly higher than that in adjacent normal gastric mucosa and was positively correlated with tumor size. Compared with GES-1 cells, the expression level of HS6ST2 in AGS and MKN45 cells was significantly elevated. Silencing HS6ST2 impaired GC cell growth, mobility and epithelial-mesenchymal transition (EMT). On the other hand, HS6ST2 upregulation increased GC cell growth, migration and invasion, which was dramatically blocked by SB431542 treatment. Furthermore, mouse xenograft experiments demonstrated that HS6ST2 silencing inhibited tumor growth and EMT in vivo.