Objective     To investigate the influence of Golgi-vesicular transport protein (p115) in gastric cancer cell line BGC-823 on the angiogenesis of gastric cancer and its possible mechanism.      Methods     BGC-823 cells were divided into a blank control group

a negative control group

and a p115 shRNA-1318-transfected group. In the p115 shRNA-transfected group

p115 shRNA-1318 was transferred into BGC-823 cells by liposome-mediated transfection. The well-transfected BGC-823 cells were screened out using G418. Western blotting was employed to analyze the protein expression levels of p115

MIF

p-Akt

and VEGF-A in BGC-823 cells. RT-PCR was employed to analyze the mRNA expression levels of p115

MIF and VEGF-A in BGC-823 cells. Cell immunofluorescence assay was employed to analyze the distributions and inhibitory rates of p115

MIF and VEGF-A in BGC-823 cells. The effect of p115 shRNA-1318-transfected BGC-823 cells on the proliferation

migration and angiogenesis of human umbilical vein endothelial cells (HUVECs) were analyzed by cellular activity assay

Transwell in vitro invasion assay

and Matrigel assay

respectively.      Results     The protein expression levels of p115

MIF

p-Akt

and VEGF-A as well as the mRNA expression levels of p115

MIF

and VEGF-A were significantly inhibited in the p115 shRNA-transfected group (P0.01). As proven by cell immunofluorescence assay

the expression levels of p115

MIF

and VEGF-A in the p115 shRNA-transfected group were significantly inhibited when compared with those in the control groups

with inhibitory rates of 63%

65%

and 68%

respectively. The proliferation rate of HUVECs in the p115 shRNA-transfected group was significantly lower than those in the control groups (P0.05). As compared with those in the control groups

the BGC-823 cells in the p115 shRNA-transfected group had significantly decreased invasion ability (P0.05). The numbers of the cells passing through Transwell chamber within 24 h in the p115 shRNA-transfected group

blank control group

and negative control group were 39±5

174±4

and 179±4

respectively. The capillary-like structures formed in the p115 shRNA-transfected group were significantly fewer than those formed in the blank control group and negative control group (422±41 vs 1 289±37 and 1 329±33

P0.05).      Conclusion     Gene silencing of p115 can down-regulate the expression of MIF and VEGF-A in gastric cancer cells and suppress the angiogenesis of gastric cancer. The molecular mechanism is probably related to the fact that MIF adjusts the angiogenesis of gastric cancer through PI3K/Akt signaling pathway.