南瓜蛋白经表皮生长因子受体信号通路诱导人胰腺癌细胞SW1990凋亡  

Cucurmosin induced the apoptosis of pancreatic cancer cell SW1990 via EGFR signaling pathway

作　　者：张宝明[1] 黄鹤光[1] 谢捷明[1] 陈明晃[2] 王丛菲[1] 殷强[1] 杨爱琴[3] 

机构地区：[1]福建医科大学附属协和医院基本外科,福州350001 [2]中国科学院福建物质结构研究所结构化学国家重点实验室 [3]福建医科大学药理学系

出　　处：《中华肝胆外科杂志》2012年第9期700-703,共4页Chinese Journal of Hepatobiliary Surgery

基　　金：国家自然科学基金（30772587）;福建省自然科学基金（C0510012,2011J01188）;福建医科大学重大科研项目（09ZD012）

摘　　要：目的探讨南瓜蛋白诱导人胰腺癌细胞SW1990凋亡的作用机制。方法Westen blot法检测表皮生长因子受体（EGFR）、P13K、Akt、Bad、Caspase-9、mTOR、P70S6K-α、4E—BPl蛋白表达水平，RT-PCR检测EGFRmRNA表达水平。结果随着药物浓度的增高，EGFR、P13K、Akt、mTOR、P70S6K—α及4E—BP1蛋白表达下调，而Bad及Caspase-9蛋白表达升高。EC；FRmRNA表达无变化。结论南瓜蛋白下调EGFR蛋白表达，并通过抑制下游P13K／Akt／mTOR信号通路，诱导人胰腺癌细胞SW1990凋亡。Objective To investigate the mechanisms involved in cucurmosin-induced apoptosis of pancreatic cancer cell SW1990. Methods The expression of EGFR, PI3K, Akt, Bad, Caspase-9, roTOR, P70S6K-a, and 4E-BP1 at the protein level were detected by western blot analysis, and RT- PCR was used to determine EGFR mRNA expression. Results An increased concentration of cucur- mosin showed a subsequent decrease in the expression of EGFR,PI3K,Akt,mTOR,P7OS6Ka, and 4E BP1, whereasthe expression of Bad and Caspase-9 were elevated. However, the mRNA expression of EGFR was unchanged. Conclusion Cucurmosin is shown to induce the apoptosis of pancreatic cancer cell SW1990 by down-regulating the expression of EGFR and thus inactivating the PI3K/Akt/ mTOR signaling pathway.

关 键 词：胰腺肿瘤 南瓜属 细胞凋亡 

分 类 号：R735.9[医药卫生—肿瘤]