论文标题
Cyclin D1的双重交易
The double dealing of cyclin D1
论文作者
论文摘要
细胞周期受细胞周期蛋白及其催化部分（Cyclin依赖性激酶（CDKS））的严格调节。 Cyclin D1与CDK4/6有关，充当有丝分裂传感器，并整合细胞外有丝分裂信号和细胞周期进程。当放松管制（过表达，积累，不合适）时，Cyclin D1变为癌基因，被公认为是实体瘤和血压的驱动力。关于细胞周期蛋白D1的致癌作用的最新研究报告了非经典功能取决于Cyclin D1及其在肿瘤细胞或组织中的位置。各种肿瘤发生的小鼠模型提供了对这些新功能的支持。最后，蛋白质组学和转录组数据确定了复杂的细胞周期蛋白D1网络。这篇综述着重于细胞周期蛋白D1病理生理学的这些方面，这对于靶向治疗可能至关重要。
The cell cycle is tightly regulated by cyclins and their catalytic moieties, the cyclin-dependent kinases (CDKs). Cyclin D1, in association with CDK4/6, acts as a mitogenic sensor and integrates extracellular mitogenic signals and cell cycle progression. When deregulated (overexpressed, accumulated, inappropriately located), cyclin D1 becomes an oncogene and is recognized as a driver of solid tumors and hemopathies. Recent studies on the oncogenic roles of cyclin D1 reported non-canonical functions dependent on the partners of cyclin D1 and its location within tumor cells or tissues. Support for these new functions was provided by various mouse models of oncogenesis. Finally, proteomic and transcriptomic data identified complex cyclin D1 networks. This review focuses on these aspects of cyclin D1 pathophysiology, which may be crucial for targeted therapy.
