Abstract:  

Objective  To investigate the effect of Fasudil on the pfoliferation， invasion and migration of gastric cancer MGC-803 cells and their probable mechanisms. Methods  MGC-803 cells were treated with different concentration of Fasudil and cell number was counted. And the subsequent experiments were conducted in 3 groups respectively contained 10， 25， 50 μmol／L of Fasudil, the MGC-803 cells treated with Fasudil were taken as the treatment group， while those not treated with Fasudil were taken as the control group. The cells were cultured for 4 days（0， 24， 48， 72， 96 h）， and the cell growth folds were detected by CCK-8.The ability of cell migration was detected by wound-healing assay. The ability of cell invasion was detected by Transwell. The protein expression levels of vascular endothelial growth factor （VEGF）， matrix metalloproteinases 9（MMP-9）， matrix metalloproteinases14 （MMP-14） and epithelial mesenchymal transformation （EMT） markers Vimentin and E-cadherin were detected by Western blotting. Results  The toxicity test showed that Fasudil inhibited the cell growth of MGC-803 cells in a dose-dependent manner and the cell growth folds were reduced in the treatment group. There was an obvious decrease in the growth folds compared to the control group （P＜0.01）. The results of wound healing assay showed that the wound closure rate in the treatment group was lower than that of the control group， and in a dose-dependent manner（P＜0.01）. Transwell results showed that the number of invasive cells in the treatment group was decreased significantly compared with the control group （P＜0.01）. Besides， Fasudil significantly decreased the expression levels of VEGF， MMP-9， MMP-14 and Vimentin， and up-regulated the expression levels of E-cadherin. Conclusion  Fasudil may inhibit cell proliferation， migration and invasion of MGC-803 cells， reduce the activity of MMP-9， MMP-14 and VEGF， which will provide new sight and theoretical basis for the treatment of gastric cancer.

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