红杉黄酮通过下调PI3K/AKT信号通路抑制胃癌细胞增殖侵袭等干细胞特性  

Sequoiaflavone inhibits stem cell properties such as proliferation and invasion of gastric cancer cells by down-regulating PI3K/AKT signaling pathway

作　　者：王艳 张金辉 赵永辰[1] 刘宏祥[1] 刘亚维 苗欢欢 杨信才[1] WANG Yan;ZHANG Jinhui;ZHAO Yongchen;LIU Hongxiang;LIU Yawei;MIAO Huanhuan;YANG Xincai(Department of Integrative Chinese and Western Medicine,Affiliated Hospital of Hebei University,Baoding 071000,Hebei,China)

机构地区：[1]河北大学附属医院中西医结合科,河北保定071000

出　　处：《中国临床药理学与治疗学》2023年第5期508-513,共6页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：河北省中医药科研计划项目(2021178)。

摘　　要：目的:探究红杉黄酮影响胃癌细胞的分子机制。方法:通过梯度浓度红杉黄酮处理胃癌细胞系AGS细胞,再使用PI3K/AKT信号通路激活剂对细胞进行诱导。采用CCK-8检测红杉黄酮对AGS细胞的最佳抑制浓度及时间,使用平板克隆、Transwell、细胞划痕实验检测细胞的增殖、迁移、侵袭能力变化。Western blot检测PI3K/AKT信号通路关键蛋白p-PI3K、PI3K、p-AKT、AKT。结果:红杉黄酮呈浓度依赖抑制AGS细胞,其半抑制浓度为0.5 mmol/L,最佳处理时间为48 h。红杉黄酮处理AGS细胞后,p-PI3K与p-AKT表达下调,AGS细胞增殖减少,迁移、侵袭能力降低;PI3K/AKT信号通路激活剂处理后,p-PI3K与p-AKT表达被部分逆转,增殖、迁移、侵袭能力降低也得到部分改善。结论:红杉黄酮通过失活PI3K/AKT信号通路抑制胃癌细胞增殖、迁移、侵袭等恶性行为。AIM:To explore the molecular mecha-nism of sequoiaflavone affecting gastric cancer cells.MEHTODS:Gastric cancer cell line AGS cells were treated with gradient concentrations of se-quoiaflavone,and then induced by PI3K/AKT signal-ing pathway activator.The optimal inhibitory con-centration and time of semi-inhibitory concentra-tion of red cedar flavonoid on AGS cells were de-tected by CCK-8,and the changes of cell prolifera-tion,migration and invasion ability were detected by colony formation assay,transwell assay and wound healing assay.PI3K/AKT signal pathway re-lated proteins p-PI3K,PI3K,p-AKT and AKT were detected by western blot.RESULTS:Sequoiaflavone inhibited AGS cells in a concentration-dependent manner.The half inhibitory concentration was 0.5 mmol/L,the optimal treatment time was 48 h.The protein expression of p-PI3K and p-AKT was down regulated.The proliferation,migration and invasion of AGS cells were decreased after treated with se-quoiaflavone.After treated with PI3K/AKT signal pathway activator,the protein expression level of p-PI3K and p-AKT was partially reversed,and the abil-ity of cell viability,proliferation,migration and inva-sion was also partially improved.CONCLUSION:In-activation of PI3K/AKT signaling pathway caused by sequoiaflavone inhibited gastric cancer cells prolif-eration,migration and invasion ability.

关 键 词：胃癌 红杉黄酮 PI3K AKT 增殖 侵袭 迁移 

分 类 号：R965.2[医药卫生—药理学]