Rosen Neal, She Qing-Bai
Department of Medicine and Program in Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.
Cancer Cell. 2006 Oct;10(4):254-6. doi: 10.1016/j.ccr.2006.10.001.
AKT, a key regulator of cell proliferation and survival, is commonly dysregulated in human cancers. Activated AKT kinase is oncogenic and required for tumorigenesis in PTEN-deficient animals. However, the importance of AKT in mediating transformation by other oncogenes and which of its targets are necessary for this process are poorly understood. In this issue of Cancer Cell, Skeen et al. show that AKT is required for transformation by mutant H-Ras and for experimental skin carcinogenesis. Moreover, the effects of AKT are mediated predominantly or solely via mTORC1. This suggests that AKT or mTOR inhibitors will be useful treatments for many cancers.
AKT是细胞增殖和存活的关键调节因子，在人类癌症中通常失调。活化的AKT激酶具有致癌性，是PTEN缺陷动物肿瘤发生所必需的。然而，AKT在介导其他致癌基因转化中的重要性以及该过程中其哪些靶点是必需的，目前尚不清楚。在本期《癌细胞》杂志中，斯金等人表明，AKT是突变型H-Ras转化和实验性皮肤癌发生所必需的。此外，AKT的作用主要或仅通过mTORC1介导。这表明AKT或mTOR抑制剂将对许多癌症有治疗作用。
