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机构地区:[1]西安医学院生物化学教研室,陕西西安710021 [2]西安交通大学生命科学与技术学院,陕西西安710049
出 处:《现代肿瘤医学》2013年第12期2666-2669,共4页Journal of Modern Oncology
基 金:陕西省教育厅科研计划资助项目(编号:12JK0711);西安医学院资助课题(编号:11FZ18)
摘 要:目的:探讨Saposin C促进PC3细胞抑癌基因p27KIP1蛋白泛素化降解,刺激细胞增殖,以及与PI3K/AKT信号通路的关系。方法:利用含有Saposin C的真核表达载体转染PC3细胞,检测Saposin C对PC3细胞Skp2、抑癌基因p27KIP1蛋白水平的调节以及对细胞增殖的影响。结果:Saposin C通过激活PI3K/AKT信号途径上调细胞内Skp2的蛋白含量,下调抑癌基因p27KIP1的蛋白水平,其机制是加速p27KIP1的蛋白降解,促进PC3细胞增殖。结论:Saposin C在PC3细胞中通过激活PI3K/AKT信号途径促进抑癌基因p27KIP1的蛋白泛素化降解,刺激细胞增殖。Objective:To investigate the effect of Saposin C on stimulation of p27KIPI degradation and stimulation of cell proliferation via PI3K/AKT signal pathway in PC3 cells. Methods:The eukaryotic expression vectors were transfected into PC3 cells containing Saposin C. Effects of Saposin C on Skp2 ,tumor suppressor gene p27KIPI protein level regulation and on PC3 cells proliferation were investigated. Results: Saposin C could upregulate Skp2 protein level and down regulate tumor suppressor gene p27KIPI protein level, its way is to accelerate the degradation of p27KIPI protein. Saposin C could also promote the proliferation of PC3 cells through activating PI3K/AKT signaling pathway. Conclusion:Saposin C could down regulate level of tumor suppressor gene p27 KIPI , accelerate its protein ubiquitina- tion and degradation via PI3K/AKT signaling pathway in PC3 cells.
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