摘 要：摘 要： PI3K的下游效应蛋白Akt，在人癌中经常处于高度激活状态。mTOR作为Akt下游的重要效应子在肿瘤发生中扮演重要角色。在PI3K-Akt-mTOR这条信号通路中，Akt所产生的效应受到两个肿瘤抑制基因的负调控：PTEN，处于Akt的上游；TSC1/TSC2，位于AKT的下游和mTOR的上游。新的研究结果表明，当缺少TSC1/TSC2的负性调节时，mTOR则通过两种复合物的平衡移动来反馈抑制Akt活性。利用小鼠遗传学手段研究PTEN和TSC2在癌症发生和进展中的角色，也证明AKT-mTOR的互相作用在癌症发展与治疗中的重要性。
关键词：蛋白激酶B；哺乳动物雷帕霉素靶体蛋白；PTEN；结节性脑硬化复合物1/2
Abstract: Abstract: The downstream effector of PI3K, Akt, is often highly-activated in human cancers. mTOR, as the downstream effector of Akt, plays pivotal role in carcinogenesis. In PI3K-Akt-mTOR signaling, Akt is negatively regulated by two tumor suppressors: PTEN, located at upstream of Akt and TSC1/TSC2 complex, lies in downstream of Akt. Latest researches indicated that Akt was regulated by a negative feedback mechanism directed by the balance of two mTOR complexes when TSC1/TSC2 was absent. The investigation of PTEN and TSC2 in carcinogenesis by mouse genetic strategies emphasizes the interplaying of Akt and mTOR in cancer research and treatment.
Key words: Akt; mTOR; PTEN; TSC1/2
