The Roles And Molecular Mechanism Of Mda-9/Syntenin In Proliferation, Invasion And Migration Of GBM Cells

ObjectiveTo investigate the effect of Syntenin on proliferation, invasion and migration of GBM cells (U-87 cells) and the molecular mechanism in this process.Methods(1) Lentiviral-mediated RNA interference was adopted to knockdown Mda-9/Syntenin expression in U-87 cells.(2) Mda-9/Syntenin mRNA expression levels were tested by real-time quantitative PCR in order to choose the best silencing sequence.(3) MTT assay was adopted to investigate the ability of cell proliferation(4) The invasion and migration ability of GBM cells were measured by Transwell assay.(5) The changes of adhesion abilities of GBM cells were measured by adhesion assay.(6) Western-blot was used to detect the expression levels of Mda-9/Syntenin, AKT, p-AKT, and MMP-9.Results(1) Relative to siRNA control cells, Mda-9/Syntenin mRNA expression level in siRAN cells which has the greatest degree of reduction was 0.18±0.07 (F<0.01)(2) Mda-9/Syntenin has no obvious effect on proliferation of U-87 cells.(3)The ability of invasion and migration was markedly reduced in siRNA cells compared with siRNA control cells, whereas, there were no significant differences between siRNA control cells and untransfected cells.(4)The adhesion ability of siRNA cells to U-87 cells was much higher than siRNA control cells, however, when they were seeded on 96-wells coated with HUVEC, the adhesion ability of siRNA cells was much lower than siRNA control cells.(5) The expression level of Mda-9/Syntenin, p-AKT, and MMP-9 in siRNA cells were markedly decreased compared with siRNA control cells. There were no significant differences in AKT expression between siRNA cells and siRNA control cells.ConclusionThe invasion and migration ability of GBM cells may be enhanced by Syntenin though its up-regulation of p-AKT, which could promote MMP-9 expression in a corresponding signal transduction pathway. However, there was no obvious effect of Mda-9/Syntenin observed on proliferation of GBM cells.