Gastric Cancer
Copyright ©The Author(s) 2002. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2002; 8(6): 994-998
Published online Dec 15, 2002. doi: 10.3748/wjg.v8.i6.994
Expression of vascular endothelial growth factor and its receptors KDR and Flt-1 in gastric cancer cells
Hua Zhang, Jian Wu, Lin Meng, Cheng-Chao Shou
Hua Zhang, Jian Wu, Lin Meng, Cheng-Chao Shou, Peking University School of Oncology, Beijing Institute for Cancer Research, Beijing 100034, China
Author contributions: All authors contributed equally to the work.
Supported by National Nature Science Foundation for Outstanding Young Scientist of China ( to S. CC., No. 39525021), National 863 program of China (2002 AA 216111) and Beijing Laboratory of Cancer Molecular Biology.
Correspondence to: Dr. Cheng-Chao Shou, Department of Biochemistry and Molecular Biology, Peking University School of Oncology, Beijing Institute for Cancer Research, No.1 Da-Hong-Luo-Chang Street, Western District, Beijing 100034, China. cshou_9@hotmail.com
Telephone: +86-10-66160960 Fax: +86-10-66175832
Received: April 25, 2002
Revised: June 2, 2002
Accepted: June 12, 2002
Published online: December 15, 2002
Abstract

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 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 VEGF121 and VEGF165 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.

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