Abstract：Objective: To explore the influence and the possible molecular mechanism of the prolyl hydroxylase(PHD)3 on clone formation and migration of gastric cancer cells. Methods: The level of PHD3 in AGS and BGC823 cell lines was up-regulated and silenced by cell transfection with overexpression plasmid or siRNA. The soft agar assay and chamber assay were used to detect the change of clone formation and migration in the gastric cancer cells. The level of Cyclin D1,c-Myc and Twist in the gastric cancer cells were measured with Western blotting. Immunofluorescence and Co-immunoprecipitation assays were used to determine the interaction between PHD3 and Dishevelled-2(DVL2). Results: After over-expressing of PHD3,the ability of clone formation and migration of AGS and BGC823 were significantly attenuated(P＜0.01). Conversely, they were significantly enhanced after silencing PHD3 (P＜0.01). Overexpression of PHD3 inhibited the level of Cyclin D1,c-Myc and Twist, down-regulated of PHD3 elevated the level of Cyclin D1,c-Myc and Twist. PHD3 and DVL2 have interaction in gastric cancer cells. Conclusion: PHD3 can restrain the clone formation and migration of gastric cancer cells by modification of β-catenin/TCF signaling.
［Key words］gastric cancer; prolyl hydroxylase 3; β-catenin/TCF signaling; clone formation and migration
2017, Vol. 27 
