Departamento de Ciências da Vida, Faculdade de Ciências e Tecnologia, Universidade Nova de Lisboa, Caparica, Portugal.
iMed.UL, Research Institute for Medicines and Pharmaceutical Sciences, Faculdade de Farmácia, Universidade de Lisboa, Lisbon, Portugal.
Drug Discov Today. 2015 Sep;20(9):1152-8. doi: 10.1016/j.drudis.2015.06.010. Epub 2015 Jun 29.
Akt2 is a pivotal player in a complex web of signaling pathways controlling cell growth, proliferation, and survival. The deregulation or aberrations of Akt2 have been associated with tumor progression, metastatic spread, and, lastly, chemoresistance. The impairment of its activity has gained more attention because Akt2 is intertwined with a range of signaling paths, including the Phosphatidylinositol 3 kinase/Akt/Mammalian target of rapamycin (PI3K/mTOR) signaling axis, which are involved in macromolecules synthesis and metabolism. Here, we focus on Akt2 because of its involvement in the acquisition of stem cell-like properties, responsible for invasiveness and chemoresistance, also promoted by Twist. We also suggest therapeutic strategies targeting Akt2 to overcome the drawbacks of current cancer therapies.
Akt2 是一个关键的角色，它参与了一个复杂的信号通路网络，这些信号通路控制着细胞的生长、增殖和存活。Akt2 的失调或异常与肿瘤的进展、转移扩散以及最后产生的化疗耐药性有关。由于 Akt2 与包括磷脂酰肌醇 3 激酶/蛋白激酶 B/哺乳动物雷帕霉素靶蛋白（PI3K/Akt/哺乳动物雷帕霉素靶蛋白，mTOR）信号轴在内的一系列信号通路相互交织，这些信号通路参与了大分子的合成和代谢，因此其活性的损害引起了更多的关注。在这里，我们专注于 Akt2，因为它参与了获得干性样特性，这一特性与侵袭性和化疗耐药性有关，也受到 Twist 的促进。我们还提出了针对 Akt2 的治疗策略，以克服当前癌症治疗的缺点。
