AIM:The expression of vascular endothelial growth factor(VEGF)and its receptors KDR and Fit-1 by gastric carcinomatissues and different gastric carcinoma cell lines was detectedto elucidate the molecular mechanism of this growth factorin promoting tumor growth.METHODS:The expression of VEGF,Fit-1 and KDR wasdetermined by reverse transcription-polymerase chainreaction(RT-PCR)in gastric cancer cell lines RF-1,RF-48,AGS-1,NCI-N87,NCI-SNU-1,NCI-SNU-5,NCI-SNU-16 andKATO-Ⅲ.The expression of Fit-1 and KDR in paraffin-embedded specimens of gastric cancer was determined byimmunohistochemistry.The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay was used toassess the role of VEGF in tumor cell proliferation.RESULTS:All 8 gastric cancer cell lines analyzed expressedVEGF_(121)and VEGF_(165)and six of them expressed both Fit-1and KDR,while cell line NCI-SNU-5 expressed Fit-1 onlyand cell line KATOⅢ expressed neither Fit-1 nor KDR.Thegastric carcinoma tissues expressed Fit-1 and KDR widely,with the positive rate of expression of Fit-1 and KDR being84.6 % and 70 % respectively.The exogenous VEGFstimulated the growth of KDR-positive cell lines NCI-N87and AGS-1 in a dose-dependent manner but exhibited noeffect on the growth of KDR-negative cell line NCI-N87.CONCLUSION:VEGF and its receptors KDR and Fit-1 wereexpressed widely in gastric carcinoma cells and the VEGFstimulated KDR-positive tumor cell growth directly.Theseresults suggest that VEGF may play a role in promoting tumorgrowth and metastasis by participating in both paracrineand autocrine pathways. AIM: The expression of vascular endothelial growth factor (VEGF) and its receptors KDR and Fit-1 by gastric carcinomatissues and different gastric carcinoma cell lines was detected to elucidate the molecular mechanism of this growth factor in promoting tumor growth. METHODS: The expression of VEGF, Fit-1 and KDR wasdetermined by reverse transcription-polymerase chain reaction (RT-PCR) in gastric cancer cell lines RF-1, RF- 48, AGS- 1, NCI- N87, NCI- SNU- 1, NCI- SNU- 5, NCI-SNU-16 and KATO-III. The expression of Fit-1 and KDR in paraffin-embedded specimens of gastric cancer was determined by immunohistochemistry. The 3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide (MTT) assay was used toassess the role of VEGF in tumor cell proliferation .RESULTS: All 8 gastric cancer cell lines analyzed expressed VEGF121 and VEGF_ (165) and six of them expressed both Fit-1and KDR, while cell line NCI- SNU-5 expressed Fit-1 only and cell line KATO III expressed neither Fit-1 nor KDR.Thegastric carcinoma tissues expressed Fit- 1 and KDR widely, with the positive rate of expression of Fit-1 and KDR being 84.6% and 70% respectively. The exogenous VEGFstimulated the growth of KDR-positive cell lines NCI-N87 and AGS-1 in a dose-dependent manner but See no no effect on the growth of KDR-negative cell line NCI-N87. CONCLUSION: VEGF and its receptors KDR and Fit-1 wereexpressed widely in gastric carcinoma cells and the VEGF stimulated KDR-positive tumor cell growth directly. These findings suggest that VEGF may play a role in promoting tumorgrowth and metastasis by participating in both paracrine and autocrine pathways.