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作 者:宋兴超 杨伟斌 韩亚民 路要武 Song Xingchao;Yang Weibin;Han Yamin;Lu Yaowu(Department of Hepatobiliary and Pancreatic Surgery,Xuzhou Municipal Hospital Affiliated to Xuzhou Medical University/Xuzhou No.1 Pelple's Hospital,Xuzhou 221000,China)
机构地区:[1]徐州医科大学附属徐州市立医院/徐州市第一人民医院肝胆胰外科,221000
出 处:《中华转移性肿瘤杂志》2021年第4期306-310,共5页Chinese Journal of Metastatic Cancer
基 金:2018年徐州医科大学校级课题(2018KJ18)
摘 要:目的探索蛋白激酶B9(AKT)抑制剂SC66对胰腺癌细胞增殖的影响及相关分子机制。方法通过生物信息学分析AKT在胰腺癌组织细胞和正常胰腺组织中的表达差异。构建AKT沉默胰腺癌细胞系。采用CCK8、蛋白印迹法及qPCR实验检测SC66对胰腺癌细胞增殖的影响及对相关细胞信号传导通路的调控和影响。结果AKT在胰腺癌组织中的表达明显升高。通过调控mTOR相关细胞信号传导通路促进胰腺癌细胞增殖,SC66通过下调AKT从而抑制胰腺癌细胞增殖。结论SC66可有效抑制胰腺癌细胞增殖,为胰腺癌的治疗提供新策略。Objective To explore the effect of protein kinase B(AKT)inhibitor SC66 on the proliferation of pancreatic cancer cells and related molecular mechanisms.Methods The expression difference of AKT in pancreatic cancer and normal pancreatic tissues was analyzed by bioinformatics.The AKT-silencing cell line was constructed,and CCK8,Western blot and qPCR experiments were performed to detect the effect of AKT inhibitor SC66 on the proliferation of pancreatic cancer cells and the regulation and influence of related cell signal transduction pathways.Results The expression of AKT in pancreatic cancer tissues was significantly increased.It promoted the proliferation of pancreatic cancer cells by regulating mTOR-related cell signaling pathways.SC66 inhibited the proliferation of pancreatic cancer cells by down-regulating AKT.Conclusion SC66 can effectively inhibit the proliferation of pancreatic cancer cells and provide a new strategy for the treatment of pancreatic cancer.
关 键 词:AKT抑制剂 AKT/mTOR信号通路 胰腺癌细胞系
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