中文摘要：

昼夜节律和细胞周期是生命有机体中两种主要的节律性、周期性的活动，参与机体代谢与生理节律．在分子水平上，它们的周期性活动是由一种周期性振荡的网络构成的，这种网络由一系列节律性表达的蛋白所形成．研究发现，多种节律因子通过调节周期蛋白的表达影响细胞周期进程，如G1-S期，REV．ERBa抑制p21促进细胞进程，RORot激活p2l抑制细胞进程，DECl抑制cyclinDl，CLOCK／BMALl负调控c-Myc；G2-M期，BMALI／CLOCK、BMALl／NPAS2或Cryl作用于耽e1抑制或激活G2-M期进程．此外，昼夜节律钟蛋白也参与了DNA损伤修复及细胞死亡的过程：Perl、Tim分别作用于ATM、ATR，因而促进细胞周期停滞，p53缺失的细胞中敲除Cry促进细胞凋亡过程，抑制了肿瘤的形成，DECl以p53依赖的方式促细胞衰老等．同时，节律因子的紊乱引起多种疾病的产生．因此，阐明昼夜节律对细胞周期及死亡的影响，将为肿瘤的治疗提供分子理论基础．

英文摘要：

Circadian rhythm and cell cycle are the two main rhythmic and cyclical activities in living organisms, where expression of a series of genes to form a regulatory network. Recent studies have revealed that various clock rhythm factors controlled cell cycle procession by regulating the expression of cell cycle proteins. For examples,the activation of p21 by RORct leads to subsequent inhibition of G1-S： transition; REV-ERBa interactions direct the inhibition of p21 to promote G1 phase progression; DEC1 inhibits cyclin D1 ; and BMAL1/CLOCK negatively regulates c-myc. G2-M through Cry to activate Weel expression. The clock rhythm protein also involved in DNA damage repair and cell death by interacting with cell cycle factors. PER1 and TIM function as cofactors for the activation of ATM or ATR ; Mutation of CRY in p53-null mice attenuates cancer onset, involving DEC1 is an effector downstream of p53 to promote premature senescence. The dysregulation of clock rhythm leads to or affects a variety of diseases, including tumors.