Icogenin对人胰腺癌BxPC3细胞侵袭转移能力的影响及其机制研究  

Effect of Icogenin on and its mechanism in anti-metastasis of pancreatic cancer BxPC3 cells

作　　者：苏富琴[1,2] 李洪燕[1] 张翼[1] 侯书杰[1] 雷平生[1] 陈晓光[1] 

机构地区：[1]中国医学科学院、北京协和医学院药物研究所,北京100050 [2]齐齐哈尔医学院药理学教研室,黑龙江齐齐哈尔161006

出　　处：《药学学报》2009年第5期456-461,共6页Acta Pharmaceutica Sinica

基　　金：国家自然科学基金资助项目(30772632)

摘　　要：观察Icogenin对人胰腺癌BxPC3细胞的体外抗转移作用,并对其作用机制进行探讨。采用穿膜方法、改良MTT法和单层细胞划痕实验观察Icogenin对BxPC3细胞侵袭、黏附和运动能力的影响。Western blotting法检测Icogenin对MAPK信号转导通路蛋白表达的变化,明胶酶法分析其对MMP2分泌的影响。结果显示,Icogenin在体外可显著抑制人胰腺癌BxPC3细胞的侵袭、运动以及黏附作用(P<0.05),并呈较好的剂量依赖关系,ERK抑制剂PD98059和U0126也可抑制侵袭转移。Icogenin可抑制MMP2的分泌,同时可抑制MAPK信号转导通路中的ERK磷酸化。因此认为Icogenin在体外具有一定的抑制胰腺癌细胞侵袭迁移的作用,其机制与抑制MMP2分泌和抑制ERK磷酸化有关。This study is to investigate the effect of Icogenin on and its mechanism in anti-metastasis of pancreatic cancer BxPC3 ceils in vitro. Using transwell assay, the effects of Icogenin on the invasion of BxPC3 cells were measured. The abilities of cell motility and adhesion in BxPC3 cells were detected by MTT assay and wound healing assay, respectively. The MAPK signal pathway protein expressions were analyzed with Western blotting. Also, the activity of MMP2 was observed by zymography assay. Icogenin inhibited the abilities of motility, adhesion and invasion of pancreatic cancer BxPC3 cells in vitro （P 〈 0.05）, in a dose-depended manner, and inhibited the secretion of MMP2 and phosphorylation of ERK. PD98059 and U0126 which were ERK inhibitors could suppress the abilities of invasion and metastasis of pancreatic cancer BxPC3 cells. It is concluded that Icogenin can inhibit the abilities of invasion and metastasis of pancreatic cancer in vitro by inhibiting the secretion of MMP2 and phosphorylation of ERK.

关 键 词：Icogenin 转移 胰腺癌细胞 

分 类 号：R963[医药卫生—微生物与生化药学]