β-Elemene inhibits the metastasis of B16F10 melanoma cells by downregulation of the expression of uPA, uPAR, MMP-2, and MMP-9

beta-Elemene has been reported to be effective for the treatment of leukemia and certain solid tumors in basic and clinical studies. However, the mechanism of action of this phytochemical remains unknown. This study aimed to investigate the effect and mechanism of beta-elemene in the mouse melanoma cell line B16F10. Cell viability was measured using the MTT assay. beta-Elemene inhibited B16F10 melanoma cell metastasis, examined using scratch and Transwell migration/invasion assays. The mRNA and protein expression of urokinase-type plasminogen activator (uPA), the uPA receptor (uPAR), matrix metalloproteinase (MMP)-2, and MMP-9 were assayed using real-time PCR, immunocytochemistry, and western blotting methods. The results indicated that beta-elemene inhibited the viability of B16F10 melanoma cells in a dose-dependent and time-dependent manner. The migratory and invasive capacities of B16F10 cells were also inhibited by beta-elemene. The expression of uPA, uPAR, MMP-2, and MMP-9 was reduced by beta-elemene at both the mRNA and protein level. beta-Elemene inhibits the metastasis of B16F10 melanoma cells through downregulation of the expression of uPA, uPAR, MMP-2, and MMP-9. Thus, beta-elemene is a natural potential anticancer drug.