Goswami Anindya, Ranganathan Padhma, Rangnekar Vivek M
Department of Radiation Medicine, University of Kentucky, Lexington, KY 40536, USA.
Cancer Res. 2006 Mar 15;66(6):2889-92. doi: 10.1158/0008-5472.CAN-05-4458.
Activation of the phosphoinositide 3-kinase (PI3K)/Akt cell survival pathway in many cancers makes it an appealing target for therapeutic development. However, because this pathway also has an important role in the survival of normal cells, tactics to achieve cancer selectivity may prove important. We recently showed that the cancer-selective proapoptotic protein Par-4 is a key target for inactivation by PI3K/Akt signaling. Additionally, we found that Par-4 participates in mediating apoptosis by PTEN, the tumor suppressor responsible for blocking PI3K/Akt signaling. As a central player in cancer cell survival, Par-4 may provide a useful focus for the development of cancer-selective therapeutics.
磷酸肌醇3激酶（PI3K）/Akt细胞存活通路在许多癌症中被激活，这使其成为治疗开发中一个有吸引力的靶点。然而，由于该通路在正常细胞存活中也起着重要作用，实现癌症选择性的策略可能被证明很重要。我们最近发现，癌症选择性促凋亡蛋白Par-4是PI3K/Akt信号传导使其失活的关键靶点。此外，我们发现Par-4参与介导由PTEN引起的细胞凋亡，PTEN是负责阻断PI3K/Akt信号传导的肿瘤抑制因子。作为癌细胞存活的核心参与者，Par-4可能为癌症选择性治疗的开发提供一个有用的焦点。
