| Objective: To investigate whether miR-126 can inhibit the invasion and metastasis of gastric cancer by regulating PI3K/ Akt /m TOR pathway over targeting GOLPH3.Methods: SGC-7901 was transfected with lentivirus to construct over expressed and suppressed miR-126 cell lines and their negative controls.Real-time fluorescence quantitative PCR was used to detect the expression lev-el of miR-126 in each group.CCK-8 and plate cloning experiments were used to detect the effects of miR-126 on the proliferation ability of SGC-7901.The effects of miR-126 on migration and invasion ability of SGC-7901 was detected by scratch test and Transwell test.The m RNA expression levels of GOLPH3,PI3 K,AKT and m TOR were detected by q RT-PCR,and the protein expression levels of GOLPH3,PI3 K,AKT,p-AKT,m TOR and p-m TOR were detected by Western blot analysis.The effect of miR-126 on the tumorigenesis ability of SGC-7901 was detected by subcutaneous tumorigenesis experiment in nude mice.Results: Cell lines with overexpression and inhibition of miR-126 were successfully constructed using SGC-7901,as well as negative control cell lines in each group.Overexpression of miR-126 inhibited the growth of SGC-7901cells(P<0.05),migration(P<0.05)and invasion(P<0.05)ability.However,inhibition the expression of miR-126 enhanced the growth of SGC-7901 cells(P<0.05),migration(P<0.05)and invasion(P<0.05)ability.Overexpression of miR-126 simultaneously down-regulated the nucleic acid and protein expression of GOLPH3,PI3 K,AKT and m-TOR(P<0.05),and the protein expression of p-AKT,p-m TOR(P<0.05);Inhibition the expression of miR-126 could enhance the nucleic acid and protein expression of GOLPH3,PI3 K,AKT and m-TOR(P<0.05),and increased the protein expression of p-AKT and p-m TOR(P<0.05).Overexpression of miR-126 can promote the tumorigenesis of SGC-7901 cells,while inhibition of miR-126 expression can prevent the tumorigenesis of each group.Conclusions: Mi R-126 can inhibit the proliferation,migration and invasion of gastric cancer cells in vitro,and inhibit the tumorigenesis of gastric cancer cells in vivo.This effect may be achieved by targeting Golph3 to regulate the PI3K/AKT/m TOR pathway. |
