论文部分内容阅读
AIM To establish the role of vascular endothelial growthfactor(VEGF)in the oncogenesis.of human gastriccarcinoma more directly.METHODS The expression of VEGF and its receptorkinase-domain insert containing receptor(KDR)in humangastric cancer tissue were observed byimmunohistochemical staining.VEGF levels weremanipulated in human gastric cancer cell using eukaryoticexpression constructs designed to express the completeVEGF_(165) complimentary DNA in either the sense orantisense orientation.The biological changes of the cellswere observed in which VEGF was up-regulated or down-regulated.RESULTS VEGF-positive rate was 50%,and VEGF wasmainly localized in the cytoplasm and membrane of thetumor cells,while KDR was mainly located in themembrane of vascular endothelial cells in gastric cancertissues and peri-cancerous tissue.In 2 cases of 50specimens,the gastric cancer cells expressed KDR,localized in both the cytoplasm and membrane.Introduction of VEGF~(165) antisense into human gastriccancer cells(SGC-7901,immunofluorescence intensity,31.6%))resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGFprotein(immunofluorescence intensity,8.9%)(P<0.05).Conversely,stable integration of VEGF_(165) inthe sense orientation resulted in an increase in cellularand cell surface VEGF(immunofluorescence intensity,75.4%)(P<0.05).Lowered VEGF levels were associatedwith a marked decrease in the growth of nude mousexenografted tumor(at 33 days postimplantation,tomorvolume:345.40 ± 136.31mm~3)(P<0.05 vs control SGC-7901 group:1534.40 ± 362.88 mm~3),whereas up-regulationof VEGF resulted in increased xenografted tumor size(at33 days postimplantation,tomor volume:2350.50 ± 637.70mm~3)(P<0.05 vs control SGC-7901 group).CONCLUSION This study provides direct evidence thatVEGF plays an important role in the oncogenesis of humangastric cancer.
AIM To establish the role of vascular endothelial growth factor(VEGF) in the oncogenesis.of human gastriccarcinoma more directly.METHODS The expression of VEGF and its receptorkinase-domain insertcontaining receptor(KDR)in human gastric cancer tissue were observed byimmunohistochemical staining.VEGF levels weremanipulated In human gastric cancer cell using eukaryotic expression constructs designed to express the completeVEGF_(165) complimentary DNA in either the sense orantisense orientation.The biological changes of the cellswere observed in which VEGF was up-regulated or downregulated.RESULTS VEGF-positive rate was 50%,and VEGF wasmainly localized in the cytoplasm and membrane of thetumor cells,while KDR was primarily located in themembrane of vascular endothelial cells in gastric cancertises and peri-cancerous tissue.In 2 cases of 50specimens,the gastric cancer cells expressed KDR,localized In both the cytoplasm and membrane.Introduction of VEGF~(165) antisense into human gastriccancer Cells(SGC-7901, immunofluorescence intensity, 31.6%))resulted in a significant reduction in VEGF-specific messenger RNA and total and cell surface VEGFprotein(immunofluorescence intensity, 8.9%)(P<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<0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mousexenografted tumor (at 33 days postimplantation, tomorvolume: 345.40 ± 136.31mm~3) (P<0.05 vs control SGC-7901 group: 1534.40 ± 362.88 mm~3), whereas up-regulationof VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tomor volume: 2350.50 ± 637.70mm~ 3)(P<0.05 vs control SGC-7901 group).CONCLUSION This study provides direct evidence that VEGF plays an important role in the oncogenesis of human gastric cancer.