Russell Robert G, Lasorella Anna, Dettin Luis E, Iavarone Antonio
Lombardi Cancer Center, Department of Oncology, Georgetown University, Washington, D. C., USA.
Cancer Res. 2004 Oct 15;64(20):7220-5. doi: 10.1158/0008-5472.CAN-04-2095.
Oncogenic signals elevate expression of Id2 in multiple tumor types. When deregulated, Id2 inactivates the tumor suppressor proteins retinoblastoma, p107, and p130. Here, we report a novel and unexpected tumor inhibitory function of Id2 in the intestinal epithelium. First, genetic ablation of Id2 in the mouse prevents differentiation and cell cycle arrest of enterocytes at the time of formation of the crypt-villus unit. Later, these developmental abnormalities evolve toward neoplastic transformation with complete penetrance. Id2-null tumors contain severe dysplastic and metaplastic lesions and express aberrant amounts of beta-catenin. Thus, our data are the first to establish a direct requirement of basic helix-loop-helix inhibitors in driving differentiation and define an unexpected role for the retinoblastoma-binding protein Id2 in preventing tumor formation.
致癌信号会提高多种肿瘤类型中Id2的表达。当Id2失调时,它会使肿瘤抑制蛋白视网膜母细胞瘤、p107和p130失活。在此,我们报告了Id2在肠上皮细胞中一种新的、意想不到的肿瘤抑制功能。首先,小鼠中Id2的基因敲除会阻止肠隐窝-绒毛单元形成时肠上皮细胞的分化和细胞周期停滞。随后,这些发育异常会完全转化为肿瘤。Id2基因缺失的肿瘤含有严重的发育异常和化生病变,并异常表达β-连环蛋白。因此,我们的数据首次证实了碱性螺旋-环-螺旋抑制剂在驱动分化中的直接需求,并确定了视网膜母细胞瘤结合蛋白Id2在预防肿瘤形成中的意想不到的作用。