Altschuler D L, Ribeiro-Neto F
Department of Pharmacology, School of Medicine, University of Pittsburgh, PA 15261, USA.
Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7475-9. doi: 10.1073/pnas.95.13.7475.
It has been widely reported that the small GTP-binding protein Rap1 has an anti-Ras and anti-mitogenic activity. Thus, it is generally accepted that a normal physiological role of Rap1 proteins is to antagonize Ras mitogenic signals, presumably by forming nonproductive complexes with proteins that are typically effectors or modulators of Ras. Rap1 is activated by signals that raise intracellular levels of cAMP, a molecule that has long been known to exert both inhibitory and stimulatory effects on cell growth. We have now tested the intriguing hypothesis that Rap1 could have mitogenic effects in systems in which cAMP stimulates cell proliferation. The result of experiments addressing this possibility revealed that Rap1 has full oncogenic potential. Expression of Rap1 in these cells results in a decreased doubling time, an increased saturation density, and an unusual anchorage-dependent morphological transformation. Most significantly, however, Rap1-expressing cells formed tumors when injected into nude mice. Thus, we propose that the view that holds Rap1 as an antimitogenic protein should be restricted and conclude that Rap1 is a conditional oncoprotein.
已有广泛报道称,小GTP结合蛋白Rap1具有抗Ras和抗有丝分裂活性。因此,人们普遍认为Rap1蛋白的正常生理作用是拮抗Ras有丝分裂信号,推测是通过与通常作为Ras效应器或调节剂的蛋白质形成无活性复合物来实现的。Rap1由提高细胞内cAMP水平的信号激活,cAMP长期以来一直被认为对细胞生长具有抑制和刺激作用。我们现在测试了一个有趣的假设,即在cAMP刺激细胞增殖的系统中,Rap1可能具有促有丝分裂作用。针对这种可能性的实验结果表明,Rap1具有完全的致癌潜力。在这些细胞中表达Rap1会导致倍增时间缩短、饱和密度增加以及一种不寻常的锚定依赖性形态转变。然而,最显著的是,表达Rap1的细胞注射到裸鼠体内时会形成肿瘤。因此,我们建议应限制将Rap1视为抗有丝分裂蛋白的观点,并得出结论,Rap1是一种条件性癌蛋白。