Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma

To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesis of human gastric carcinoma more directly. The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF le...

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Veröffentlicht in:World journal of gastroenterology : WJG 2001-08, Vol.7 (4), p.500-505
Hauptverfasser: Liu, D H, Zhang, X Y, Fan, D M, Huang, Y X, Zhang, J S, Huang, W Q, Zhang, Y Q, Huang, Q S, Ma, W Y, Chai, Y B, Jin, M
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container_title World journal of gastroenterology : WJG
container_volume 7
creator Liu, D H
Zhang, X Y
Fan, D M
Huang, Y X
Zhang, J S
Huang, W Q
Zhang, Y Q
Huang, Q S
Ma, W Y
Chai, Y B
Jin, M
description To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesis of human gastric carcinoma more directly. The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF(165) complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or down-regulated. VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR, localized in both the cytoplasm and membrane. Introduction of VEGF(165) antisense into human gastric cancer cells (SGC-7901, immunofluorescence intensity, 31.6%)) resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGF protein (immunofluorescence intensity, 8.9%) (P
doi_str_mv 10.3748/wjg.v7.i4.500
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The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF(165) complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or down-regulated. VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR, localized in both the cytoplasm and membrane. Introduction of VEGF(165) antisense into human gastric cancer cells (SGC-7901, immunofluorescence intensity, 31.6%)) resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGF protein (immunofluorescence intensity, 8.9%) (P&lt;0.05). Conversely, stable integration of VEGF(165) in the sense orientation resulted in an increase in cellular and cell surface VEGF (immunofluorescence intensity, 75.4%) (P&lt;0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mouse xenografted tumor (at 33 days postimplantation, tumor volume: 345.40 +/- 136.31 mm3)(P&lt;0.05 vs control SGC-7901 group: 1534.40 +/- 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tumor volume: 2350.50 +/- 637.70 mm3) (P&lt;0.05 vs control SGC-7901 group). This study provides direct evidence that VEGF plays an important role in the oncogenesis of human gastric cancer.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.v7.i4.500</identifier><identifier>PMID: 11819817</identifier><language>eng</language><publisher>United States: lnstitute of Digestive Disease, Xijing Hospital%Department of Gastroenterology, Tangdu Hospital%Department of Histology and Embryology%Department of Microbiology%Department of Biochemistry, Fourth Military Medical University, Xi an 710033,Shaanxi Province, China</publisher><subject>Adult ; Aged ; Animals ; Cell Division ; Cloning, Molecular ; DNA, Antisense ; DNA, Complementary ; Endothelial Growth Factors - genetics ; Endothelium, Vascular - physiology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphokines - genetics ; Male ; Mice ; Mice, Nude ; Middle Aged ; Neovascularization, Pathologic - pathology ; Neovascularization, Pathologic - physiopathology ; Original Research ; Receptor Protein-Tyrosine Kinases - genetics ; Receptors, Growth Factor - genetics ; Receptors, Vascular Endothelial Growth Factor ; Stomach Neoplasms - pathology ; Stomach Neoplasms - physiopathology ; Transfection ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>World journal of gastroenterology : WJG, 2001-08, Vol.7 (4), p.500-505</ispartof><rights>Copyright © Wanfang Data Co. 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The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF(165) complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or down-regulated. VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR, localized in both the cytoplasm and membrane. Introduction of VEGF(165) antisense into human gastric cancer cells (SGC-7901, immunofluorescence intensity, 31.6%)) resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGF protein (immunofluorescence intensity, 8.9%) (P&lt;0.05). Conversely, stable integration of VEGF(165) in the sense orientation resulted in an increase in cellular and cell surface VEGF (immunofluorescence intensity, 75.4%) (P&lt;0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mouse xenografted tumor (at 33 days postimplantation, tumor volume: 345.40 +/- 136.31 mm3)(P&lt;0.05 vs control SGC-7901 group: 1534.40 +/- 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tumor volume: 2350.50 +/- 637.70 mm3) (P&lt;0.05 vs control SGC-7901 group). 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The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF(165) complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or down-regulated. VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR, localized in both the cytoplasm and membrane. Introduction of VEGF(165) antisense into human gastric cancer cells (SGC-7901, immunofluorescence intensity, 31.6%)) resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGF protein (immunofluorescence intensity, 8.9%) (P&lt;0.05). Conversely, stable integration of VEGF(165) in the sense orientation resulted in an increase in cellular and cell surface VEGF (immunofluorescence intensity, 75.4%) (P&lt;0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mouse xenografted tumor (at 33 days postimplantation, tumor volume: 345.40 +/- 136.31 mm3)(P&lt;0.05 vs control SGC-7901 group: 1534.40 +/- 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tumor volume: 2350.50 +/- 637.70 mm3) (P&lt;0.05 vs control SGC-7901 group). This study provides direct evidence that VEGF plays an important role in the oncogenesis of human gastric cancer.</abstract><cop>United States</cop><pub>lnstitute of Digestive Disease, Xijing Hospital%Department of Gastroenterology, Tangdu Hospital%Department of Histology and Embryology%Department of Microbiology%Department of Biochemistry, Fourth Military Medical University, Xi an 710033,Shaanxi Province, China</pub><pmid>11819817</pmid><doi>10.3748/wjg.v7.i4.500</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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ispartof World journal of gastroenterology : WJG, 2001-08, Vol.7 (4), p.500-505
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source MEDLINE; PubMed Central; Alma/SFX Local Collection
subjects Adult
Aged
Animals
Cell Division
Cloning, Molecular
DNA, Antisense
DNA, Complementary
Endothelial Growth Factors - genetics
Endothelium, Vascular - physiology
Female
Gene Expression Regulation, Neoplastic
Humans
Lymphokines - genetics
Male
Mice
Mice, Nude
Middle Aged
Neovascularization, Pathologic - pathology
Neovascularization, Pathologic - physiopathology
Original Research
Receptor Protein-Tyrosine Kinases - genetics
Receptors, Growth Factor - genetics
Receptors, Vascular Endothelial Growth Factor
Stomach Neoplasms - pathology
Stomach Neoplasms - physiopathology
Transfection
Tumor Cells, Cultured
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
title Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma
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