AIM:To investigate the effects of mifepristone on the invasiveand metastatic potential of human gastric adenocarcinomacell line MKN-45 and its mechanisms.METHODS:After incubation with various concentrations ofmifepristone(5,10,20 μmol/L),the adhesion to artificialbasement membrane,Matrigel,and the migration of MKN-45cells were assayed using MTT assay and Transwell cell culturechambers,respectively.Enzyme- linked immunoabsorbentassay(ELISA)and flow Oltometry were used to determinethe expression of vascular endothelial growth factor(VEGF)and integrin β3 in the cells.After subcutaneous transplantationof MKN-45 cells in nude mice,mifepristone(50 mg/kg·d)was administrated subcutaneously for 8 wk to assess itseffects on tumor metastasis,immunohistochemical analysiswas used to detect the expression of VEGF and microvasculardensity(MVD)in xenografted tumors.RESULTS:Mifepristone dose-dependently inhibited theheterotypic adhesion to Matrigel of MKN-45 cells.Theinhibition was accompanied by a significant down-regulationof integrin β3 expression in the cells.After incubation with5,10,20μmol/L mifepristone,the number of migrated MKN-45 cells was 72±8,50±6,41±5 in experiment group,and94±16 in control group(P<0.01).Meanwhile,secreted VEGFprotein of MKN-45 cells in mifepristone-treated group(14.2±2.9,8.9±3.1,5.4±2.1 ng/g per liter)was significantlylower than that in control group(22.7±4.3 ng/g per liter,P<0.01).In vivo,mifepristone decreased the number ofmetastatic foci in lungs of nude mice and down-regulatedthe expression of VEGF and MVD in the xenograted tumors.CONCLUSION:Mifepristone can effectively inhibit theinvasive and metastatic potential of human gastricadenocarcinoma cell line MKN-45 in vitro and in vivo throughinhibition of heterotypic adhesion to basement membrane,cell migration and angiogenesis. AIM: To investigate the effects of mifepristone on the invasive and metastatic potential of human gastric adenocarcinoma cell line MKN-45 and its mechanisms. METHODS: After incubation with various concentrations of mifepristone (5, 10, 20 μmol / L) Matrigel, and the migration of MKN-45 cells were assayed using MTT assay and Transwell cell culture chambers, respectively. Enzyme-linked immunoabsorbent assay (ELISA) and flow Oltometry were used to determine the expression of vascular endothelial growth factor (VEGF) and integrin β3 in the cells . After subcutaneous transplantation of MKN-45 cells in nude mice, mifepristone (50 mg / kg · d) was administered subcutaneously for 8 weeks to assess itseffects on tumor metastasis, immunohistochemical analysiswas used to detect the expression of VEGF and microvasculardensity (MVD) in xenografted tumors.RESULTS: Mifepristone dose-dependently inhibited theheterotypic adhesion to Matrigel of MKN-45 cells. The inhibition was accompanied by a significant down-regulation of integrin β3 expression in the cells. After incubation with 5, 10, 20 μmol / L mifepristone, the number of migrated MKN-45 cells was 72 ± 8,50 ± 6,41 ± 5 in experiment group, and 94 ± 16 in control group (P <0.01). While, the significant VEGFprotein of MKN-45 cells in mifepristone-treated group (14.2 ± 2.9,8.9 ± 3.1,5.4 ± 2.1 ng / g per liter) was significantlylower than that in control group (22.7 ± 4.3 ng / g per liter, P <0.01). In vivo, mifepristone decreased the number of metastatic foci in lungs of nude mice and down-regulated the expression of VEGF and MVD in the xenograted tumors. CONCLUSION: Mifepristone can effectively inhibit the invasive and metastatic potential of human gastricadenocarcinoma cell line MKN-45 in vitro and in vivo through inhibition of heterotypic adhesion to basement membrane, cell migration and angiogenesis.