咖啡因通过FAK/AKT/ROCK通路调控人脑胶质瘤U-373MG细胞的恶性生物学行为OA北大核心CSTPCD

Objective:To investigate the effects of caffeine on the proliferation,migration and invasion abilities of human brain glioma U-373MG cells by regulating the FAK/AKT/ROCK signaling pathway.Methods:U-373MG cells were routinely cultured and divided into the control group,the low dose caffeine(1 mmol/L)group,the high dose caffeine(2 mmol/L)group,the PF573228 group(FAK inhibitor,1 μmol/L),and the high dose caffeine+SC79 group(AKT activator,8 mg/L).The proliferation ability,migration ability,invasion ability and apoptosis rate of U-373MG cells in each group as well as the expression levels of p-FAK,p-AKT,p-ROCK,Ki67 and MMP-9 proteins in U-373MG cells were detected by CCK-8,Transwell assay,flow cytometry and WB assay,respectively.A U-373MG cell nude mouse model was established to observe the effect of caffeine on the growth of transplanted tumor.The expressions of related proteins in transplanted tumor tissues were detected by WB method.Results:Caffeine and PF573228 could significantly inhibit the proliferation,migration and invasion abilities of U-373MG cells,promote apoptosis of U-373MG cells,and inhibit the expressions of p-FAK,p-Akt,p-Rock,Ki67 and MMP-9 proteins(all P<0.05).SC79 could partially reverse the effect of caffeine on U-373MG cells.Caffeine could significantly inhibit the growth of transplanted tumors and the expressions of above related proteins in transplanted tumor tissues(all P<0.05).Conclusion:Caffeine can inhibit the proliferation,migration and invasion abilities of U-373MG cells and promote their apoptosis by inhibiting the FAK/AKT/ROCK signaling pathway.