Figure 6.

Effect of the inhibition of PI3K activation on co-cultured cell CCL-2 expression, invasion and migration. (A) Reverse transcription-quantitative polymerase chain reaction and (B) western blot analysis determined that, following co-culture with MC, the relative expression of CCL-2 mRNA and protein in gastric cancer cells was increased, compared with the control. However, if cells were pre-treated with the specific PI3K inhibitor wortmannin, the increase in the gene and protein expression levels of CCL-2 was significantly inhibited. GADPH was used as the loading control. (C) Migration and (D) invasion assays demonstrating that the migration of gastric cancer cells increased with MC co-culture, but decreased following the addition of the PI3K inhibitor wortmannin. ***P<0.001 MC vs. CTL; ^#P<0.05, ^##P<0.01 and ^###P<0.001 MC vs. MC+ inhibitor. PI3K, phosphoinositide 3-kinase; CCL-2, C-C motif chemokine ligand 2; CCR2, C-C motif chemokine receptor 2; MC, mast cell co-culture group; CTL, control group.