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AIM:To estimate whether STI571 inhibits the expressionof vascular endothelial growth factor(VEGF)in thegastrointestinal stromal tumor(GIST)cells.METHODS:We used GIST cell line,GIST-T1.It hasa heterogenic 57-bp deletion in exon 11 to produce amutated c-KIT,which results in constitutive activationof c-KIT.Cells were treated with/without STI571 orstem cell factor(SCF).Transcription and expression ofVEGF were determined by RT-PCR and flow cytometryor Western blotting,respectively.Activated c-KIT wasestimated by immunoprecipitation analysis.Cell viabilitywas determined by MTT assay.RESULTS:Activation of c-KIT was inhibited bySTI571 treatment.VEGF was suppressed at both thetranscriptional and translational levels in a temporal anddose-dependent manner by STI571.SCF upregulatedthe expression of VEGF and it was inhibited by STI571.STI571 also reduced the cell viability of the GIST-T1cells,as determined by MTT assay.CONCLUSION:Activation of c-KIT in the GIST-T1regulated the expression of VEGF and it was inhibited bySTI571.STI571 has antitumor effects on the GIST cellswith respect to not only the inhibition of cell growth,butalso the suppression of VEGF expression.
AIM: To assess whether STI571 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 hasa heterogenic 57-bp deletion in exon 11 to produce amutated c-KIT, which results in constitutive activation of c-KIT.Cells were treated with / without STI571 orstem cell factor (SCF). Transcription and expression of VEGF were determined by RT-PCR and flow cytometryor Western blot, respectively. Activated c-KIT wasestimated by immunoprecipitation analysis. Cell viability was determined by MTT assay. RESULTS: Activation of c-KIT was inhibited by STI571 treatment. VEGF was suppressed at both the transcription and translational levels in a temporal and dependent-dependent manner by STI571. SCF upregulated the expression of VEGF and it was inhibited by STI571.STI571 also reduced the cell viability of the GIST-T1 cells, as determined by MTT assay. CONCLUSION: Activation of c-KIT in the GIST-T1 regulated expression of VEGF a nd it was inhibited by STI571.STI571 has antitumor effects on the GIST cells with respect to not only the inhibition of cell growth, butalso the suppression of VEGF expression.