Ray Dipankar, Kiyokawa Hiroaki
Department of Molecular Pharmacology and Biological Chemistry, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL 60611, USA.
Cancer Res. 2008 Mar 1;68(5):1251-3. doi: 10.1158/0008-5472.CAN-07-5983.
CDC25A is a critical regulator of cell cycle progression and checkpoint response. Overexpression of this cyclin-dependent kinase phosphatase occurs often in human cancers. Our recent genetic studies in the mouse indicate that restricting CDC25A can limit tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell division or viability. These findings offer a sound foundation to justify development of CDC25A inhibitors for antitumor therapy.
细胞周期蛋白依赖性激酶25A(CDC25A)是细胞周期进程和检查点反应的关键调节因子。这种细胞周期蛋白依赖性激酶磷酸酶的过表达在人类癌症中经常出现。我们最近在小鼠身上进行的遗传学研究表明,限制CDC25A可以限制由HER2/neu-RAS致癌途径诱导的肿瘤发生,而不会损害正常细胞分裂或活力。这些发现为开发用于抗肿瘤治疗的CDC25A抑制剂提供了坚实的基础。