Ruley H E
Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.
Cancer Cells. 1990 Aug-Sep;2(8-9):258-68.
Nuclear proteins encoded by both cellular oncogenes and DNA tumor viruses enable activated ras oncogenes to transform a variety of cell types to a tumorigenic state. The interactions are complementary, suggesting that collaborating oncogenes release cells from controls that preclude transformation by ras alone. The nuclear oncoproteins bind both protein and nucleic acid targets and affect processes important in transcription and cell cycle control. Transforming collaborations between oncogenes provide a genetic context to study biochemical interactions involved in normal growth control and to identify mechanisms important in multistep carcinogenesis.
细胞癌基因和DNA肿瘤病毒编码的核蛋白能使激活的ras癌基因将多种细胞类型转化为致瘤状态。这些相互作用是互补的,这表明协同作用的癌基因使细胞摆脱了仅由ras介导转化时所受到的限制。核癌蛋白既能结合蛋白质靶点,也能结合核酸靶点,并影响转录和细胞周期调控中重要的过程。癌基因之间的转化协同作用提供了一个遗传学背景,用于研究正常生长调控中涉及的生化相互作用,并确定在多步骤致癌过程中起重要作用的机制。