mTORC2/Akt的反馈激活可拮抗隐丹参酮对HepG2细胞的抑制作用  

Feedback Activation of mTORC2/Akt Restrain Cryptotanshinone-Induced Inhibition of HepG2 Cell Proliferation

作　　者：洪鎏[1,2] 李山虎[1] 王洪涛[1] 黄芳[1] 王健[1] 王芃[1] 吕文杰[2] 潘耀振[2] 周建光[1] 

机构地区：[1]军事医学科学院生物工程研究所,北京100850 [2]贵阳医学院附属医院,贵州贵阳550001

出　　处：《生物技术通讯》2015年第1期51-54,共4页Letters in Biotechnology

基　　金：国家自然科学基金(81470138;81172445;81372140)

摘　　要：目的:研究隐丹参酮对Akt活性的影响及其在抑制HepG2细胞生长中的作用。方法:Western印迹检测隐丹参酮对Akt磷酸化的影响;CCK-8法检测隐丹参酮与MK2206或PP242联合用药对HepG2的生长抑制作用。结果:Western印迹证明隐丹参酮处理能够增强HepG2细胞Akt的磷酸化,同时发现隐丹参酮对Akt的增强作用依赖于mTORC2的活性;通过MK2206或PP242抑制Akt的反馈激活,能够明显促进隐丹参酮对HepG2细胞的生长抑制作用。结论:通过抑制Akt的反馈激活能够增强隐丹参酮的抗肿瘤作用,为隐丹参酮肿瘤治疗的临床应用联合用药提供了理论基础。Objective： To study the influence of cryptotanshinone（CPT） on Akt activity and the role which plays in the HepG2 cell growth inhibited by CPT. Methods： Western blotting was used to detect the effect of CPT on phosphorylation of Akt. CCK-8 was used to examine the inhibition of HepG2 cell growth treated by the combination of CPT and MK2206 or PP242. Results： The enhanced phosphorylation of Akt stimulated by CPT in HepG2 cell was identified by Western blotting, and this process was found depending on the activity of mTORC2. The inhibition of HepG2 cell growth was significantly enhanced by Akt loopback treated with Akt inhibitor MK2206 or roTOR inhibitor PP242 combined with CPT. Conclusion： The anti-tumor function of CPT was enhanced by inhibition of Akt loopback, which makes the theoretical basis for clinical medication.

关 键 词：AKT 隐丹参酮 肝癌 HEPG2细胞 

分 类 号：Q25[生物学—细胞生物学]