Pucci B, Kasten M, Giordano A
Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Neoplasia. 2000 Jul-Aug;2(4):291-9. doi: 10.1038/sj.neo.7900101.
In multicellular organisms, cell proliferation and death must be regulated to maintain tissue homeostasis. Many observations suggest that this regulation may be achieved, in part, by coupling the process of cell cycle progression and programmed cell death by using and controlling a shared set of factors. An argument in favor of a link between the cell cycle and apoptosis arises from the accumulated evidence that manipulation of the cell cycle may either prevent or induce an apoptotic response. This linkage has been recognized for tumor suppressor genes such as p53 and RB, the dominant oncogene, c-Myc, and several cyclin-dependent kinases (Cdks) and their regulators. These proteins that function in proliferative pathways may also act to sensitize cells to apoptosis. Indeed, unregulated cell proliferation can result in pathologic conditions including neoplasias if it is not countered by the appropriate cell death. Translating the knowledge gained by studying the connection between cell death and cell proliferation may aid in identifying novel therapies to circumvent disease progression or improve clinical outcome.
在多细胞生物体中，必须调节细胞增殖和死亡以维持组织稳态。许多观察结果表明，这种调节可能部分是通过利用和控制一组共享因子来耦合细胞周期进程和程序性细胞死亡过程来实现的。支持细胞周期与细胞凋亡之间存在联系的一个论据来自于积累的证据，即对细胞周期的操纵可能会预防或诱导凋亡反应。这种联系已在肿瘤抑制基因如p53和RB、主要癌基因c-Myc以及几种细胞周期蛋白依赖性激酶（Cdks）及其调节因子中得到认可。这些在增殖途径中起作用的蛋白质也可能使细胞对凋亡敏感。事实上，如果不受适当的细胞死亡的对抗，不受控制的细胞增殖会导致包括肿瘤形成在内的病理状况。将通过研究细胞死亡与细胞增殖之间的联系所获得的知识转化应用，可能有助于确定新的疗法，以规避疾病进展或改善临床结果。
