AIM： To estimate whether S-TI571 inhibits the expression of vascular endothelial growth factor （VEGF） in the gastrointestinal stromal tumor （GIST） cells. METHODS： We used GIST cell line, GIST-T1. It has a hetero...AIM： To estimate whether S-TI571 inhibits the expression of vascular endothelial growth factor （VEGF） in the gastrointestinal stromal tumor （GIST） cells. METHODS： We used GIST cell line, GIST-T1. It has a heterogenic 57-bp deletion in exon 11 to produce a mutated c-KIT, which results in constitutive activation of c-KIT. Cells were treated with/without STI571 or stem cell factor （SCF）. Transcription and expression of VEGF were determined by RT-PCR and flow cytometry or Western blotting, respectively. Activated c-KIT was estimated by immunoprecipitation analysis. Cell viability was determined by PITT assay. RESULTS： Activation of c-KIT was inhibited by STI571 treatment. VEGF was suppressed at both the transcriptional and translational levels in a temporal and dose-dependent manner by STI571. SCF upregulated the expression of VEGF and it was inhibited by S-13571. STI571 also reduced the cell viability of the GIST-T1 cells, as determined by PTT assay. CONCLUSION： Activation of c-KIT in the GIST-T1 regulated the expression of VEGF and it was inhibited by ST571. STI571 has antitumor effects on the GIST cells with respect to not only the inhibition of cell growth, but also the suppression of VEGF expression.展开更多
目的探讨格列卫(Gleevec or Glivec,代号STI571)在体外对人胃肠道间质瘤-T1细胞(GIST-T1)血管内皮生长因子(VEGF)表达的影响。方法体外培养人胃肠道间质瘤-T1细胞,MTT法检测格列卫对人胃肠道间质瘤-T1细胞的增殖抑制作用,RT—PCR方法检...目的探讨格列卫(Gleevec or Glivec,代号STI571)在体外对人胃肠道间质瘤-T1细胞(GIST-T1)血管内皮生长因子(VEGF)表达的影响。方法体外培养人胃肠道间质瘤-T1细胞,MTT法检测格列卫对人胃肠道间质瘤-T1细胞的增殖抑制作用,RT—PCR方法检测VEGF mRNA表达,Western blot检测VEGF蛋白表达水平的变化。结果格列卫呈剂量性抑制人胃肠道间质瘤-T1细胞;人胃肠道间质瘤-T1细胞高水平表达VEGF,格列卫能显著降低人胃肠道间质瘤-T1细胞VEGF mRNA和蛋白表达。结论格列卫可以下调人胃肠道间质瘤-T1细胞VEGF的表达,进一步抑制人胃肠道间质瘤-T1细胞的增殖。展开更多
文摘AIM： To estimate whether S-TI571 inhibits the expression of vascular endothelial growth factor （VEGF） in the gastrointestinal stromal tumor （GIST） cells. METHODS： We used GIST cell line, GIST-T1. It has a heterogenic 57-bp deletion in exon 11 to produce a mutated c-KIT, which results in constitutive activation of c-KIT. Cells were treated with/without STI571 or stem cell factor （SCF）. Transcription and expression of VEGF were determined by RT-PCR and flow cytometry or Western blotting, respectively. Activated c-KIT was estimated by immunoprecipitation analysis. Cell viability was determined by PITT assay. RESULTS： Activation of c-KIT was inhibited by STI571 treatment. VEGF was suppressed at both the transcriptional and translational levels in a temporal and dose-dependent manner by STI571. SCF upregulated the expression of VEGF and it was inhibited by S-13571. STI571 also reduced the cell viability of the GIST-T1 cells, as determined by PTT assay. CONCLUSION： Activation of c-KIT in the GIST-T1 regulated the expression of VEGF and it was inhibited by ST571. STI571 has antitumor effects on the GIST cells with respect to not only the inhibition of cell growth, but also the suppression of VEGF expression.
