紫铆因调控PI3K/AKT通路抑制人胃癌细胞增殖

Effect of Butein on the Proliferation of Gastric Cancer Cells

为了探讨紫铆因对胃癌细胞增殖的影响及作用机制。本研究用15μmol/L、30μmol/L和60μmol/L的紫铆因处理MGC803细胞后,运用CCK-8法检测细胞增殖情况,采用流式细胞术检测细胞周期分布情况,使用Western blotting检测Cyclin B1、CDK1、p-PI3K、p-AKT、PI3K和AKT蛋白表达水平。研究表明:15μmol/L、30μmol/L和60μmol/L的紫铆因处理48 h和72 h后,MGC803细胞增殖能力明显降低(p<0.05)。15μmol/L、30μmol/L和60μmol/L的紫铆因作用细胞48 h后,处于G2/M期的MGC803细胞数量显著增加(p<0.05)。15μmol/L、30μmol/L和60μmol/L的紫铆因作用MGC803细胞48 h后,Cyclin B1和CDK1蛋白表达水平明显降低(p<0.05)。此外,15μmol/L、30μmol/L和60μmol/L的紫铆因作用48 h后,MGC803细胞磷酸化PI3K和AKT蛋白表达水平显著降低(p<0.05)。研究结果显示:紫铆因通过抑制PI3K/AKT通路的活化从而抑制人胃癌细胞增殖。

To explore the effect and possible mechanism of Butein on the proliferation of human gastric carcinoma cells.In this research,CCK-8 assay was applied to detect the proliferation.Flow cytometry was used to detect cell cycle distribution.Western blotting assay was used to determine the expression levels of Cyclin B1,CDK1,p-PI3K,p-AKT,PI3K as well as AKT proteins.The cell proliferation.ability of MGC803 cells were significantly decreased after treatment with 15μmol/L,30μmol/L or 60μmol/L of Butein for 48 h and 72 h.Besides,the cell numbers in G2/M period was significantly accumulated and the expression levels of Cyclin B1 and CDK1 proteins were obviously reduced inMGC803 cells treated with Butein(15μmol/L,30μmol/L or 60μmol/L)for 48 h.We also found that the levels of phosphorylated PI3K and AKT proteins were markedly downregulated in MGC803 cells exposured to Butein(15μmol/L,30μmol/L or 60μmol/L)for 48 h.The preliminary conclusion of this study comfirmed that Butein inhibits gastric cancer cell proliferation by inhibiting the activation of PI3K/AKT pathway.