Expression of vascular endothelial growth factor and its receptors KDR and Fit-1 in gastric cancer cells

AIM: The expression of vascular endothelial growth factor (VEGF) and its receptors KDR and Flt-1 by gastric carcinoma tissues 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, Flt-1 and KDR was determined 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 Flt-1 and KDR in paraffinembedded specimens of gastric cancer was determined by immunohistochemistry. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to assess the role of VEGF in tumor cell proliferation.RESULTS: All 8 gastric cancer cell lines analyzed expressed VEGF121 and VEGF16s and six of them expressed both Flt-1 and KDR, while cell line NCI-SNU-5 expressed Flt-1 only and cell line KATOⅢ expressed neither Flt-1 nor KDR. The gastric carcinoma tissues expressed Flt-1 and KDR widely,with the positive rate of expression of Flt-1 and KDR being 84.6 % and 70 % respectively. The exogenous VEGF stimulated the growth of KDR-positive cell lines NCI-N87 and AGS-1 in a dose-dependent manner but exhibited no effect on the growth of KDR-negative cell line NCI-N87.CONCLUSION: VEGF and its receptors KDR and Flt-1 were expressed widely in gastric carcinoma cells and the VEGF stimulated KDR-positive tumor cell growth directly. These results suggest that VEGF may play a role in promoting tumor growth and metastasis by participating in both paracrine and autocrine pathways.

AIM:The expression of vascular endothelial growth factor (VEGF)and its receptors KDR and Fit-1 by gastric carcinoma tissues 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 was determined 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 to assess the role of VEGF in tumor cell proliferation. RESULTS:All 8 gastric cancer cell lines analyzed expressed VEGF_(121)and VEGF_(165)and six of them expressed both Fit-1 and KDR,while cell line NCI-SNU-5 expressed Fit-1 only and cell line KATOⅢ expressed neither Fit-1 nor KDR.The gastric 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 VEGF stimulated the growth of KDR-positive cell lines NCI-N87 and AGS-1 in a dose-dependent manner but exhibited no effect on the growth of KDR-negative cell line NCI-N87. CONCLUSION:VEGF and its receptors KDR and Fit-1 were expressed widely in gastric carcinoma cells and the VEGF stimulated KDR-positive tumor cell growth directly.These results suggest that VEGF may play a role in promoting tumor growth and metastasis by participating in both paracrine and autocrine pathways.