Cross-talk between the circadian clock and the cell cycle in cancer

被引:123
作者
Sotak, Matus [1 ]
Sumova, Alena [1 ]
Pacha, Jiri [1 ]
机构
[1] Acad Sci Czech Republ, Inst Physiol, Prague 14220 4, Czech Republic
关键词
Apoptosis; cancer; cell cycle; circadian clock; MAPK cascade; proliferation; Wnt signaling; EPIDERMAL-GROWTH-FACTOR; CHECKPOINT KINASE WEE1; NIGHT-SHIFT WORK; BREAST-CANCER; DNA-DAMAGE; TRANSCRIPTION FACTOR; INHIBITS GROWTH; GENE-EXPRESSION; CONSTANT LIGHT; STEM-CELL;
D O I
10.3109/07853890.2014.892296
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The circadian clock is an endogenous timekeeper system that controls the daily rhythms of a variety of physiological processes. Accumulating evidence indicates that genetic changes or unhealthy lifestyle can lead to a disruption of circadian homeostasis, which is a risk factor for severe dysfunctions and pathologies including cancer. Cell cycle, proliferation, and cell death are closely intertwined with the circadian clock, and thus disruption of circadian rhythms appears to be linked to cancer development and progression. At the molecular level, the cell cycle machinery and the circadian clocks are controlled by similar mechanisms, including feedback loops of genes and protein products that display periodic activation and repression. Here, we review the circadian rhythmicity of genes associated with the cell cycle, proliferation, and apoptosis, and we highlight the potential connection between these processes, the circadian clock, and neoplastic transformations. Understanding these interconnections might have potential implications for the prevention and therapy of malignant diseases.
引用
收藏
页码:221 / 232
页数:12
相关论文
共 133 条
[1]   p21 in cancer: intricate networks and multiple activities [J].
Abbas, Tarek ;
Dutta, Anindya .
NATURE REVIEWS CANCER, 2009, 9 (06) :400-414
[2]   Control of intracellular dynamics of mammalian period proteins by casein kinase I ε (CKIε) and CKIδ in cultured cells [J].
Akashi, M ;
Tsuchiya, Y ;
Yoshino, T ;
Nishida, E .
MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (06) :1693-1703
[3]   Myc suppresses induction of the growth arrest genes gadd34, gadd45, and gadd153 by DNA-damaging agents [J].
Amundson, SA ;
Zhan, Q ;
Penn, LZ ;
Fornace, AJ .
ONCOGENE, 1998, 17 (17) :2149-2154
[4]   WNT signalling pathways as therapeutic targets in cancer [J].
Anastas, Jamie N. ;
Moon, Randall T. .
NATURE REVIEWS CANCER, 2013, 13 (01) :11-26
[5]   Effect of constant light on DMBA mammary tumorigenesis in rats [J].
Anderson, LE ;
Morris, JE ;
Sasser, LB ;
Stevens, RG .
CANCER LETTERS, 2000, 148 (02) :121-126
[6]   Gene Ontology: tool for the unification of biology [J].
Ashburner, M ;
Ball, CA ;
Blake, JA ;
Botstein, D ;
Butler, H ;
Cherry, JM ;
Davis, AP ;
Dolinski, K ;
Dwight, SS ;
Eppig, JT ;
Harris, MA ;
Hill, DP ;
Issel-Tarver, L ;
Kasarskis, A ;
Lewis, S ;
Matese, JC ;
Richardson, JE ;
Ringwald, M ;
Rubin, GM ;
Sherlock, G .
NATURE GENETICS, 2000, 25 (01) :25-29
[7]   Differential functions of mPer1, mPer2, and mPer3 in the SCN circadian clock [J].
Bae, K ;
Jin, XW ;
Maywood, ES ;
Hastings, MH ;
Reppert, SM ;
Weaver, DR .
NEURON, 2001, 30 (02) :525-536
[8]   Control of cell cycle transcription during G1 and S phases [J].
Bertoli, Cosetta ;
Skotheim, Jan M. ;
de Bruin, Robertus A. M. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2013, 14 (08) :518-528
[9]   Regulation of cell cycle checkpoint kinase WEE1 by miR-195 in malignant melanoma [J].
Bhattacharya, A. ;
Schmitz, U. ;
Wolkenhauer, O. ;
Schoenherr, M. ;
Raatz, Y. ;
Kunz, M. .
ONCOGENE, 2013, 32 (26) :3175-3183
[10]   Circadian variation in the expression of cell-cycle proteins in human oral epithelium [J].
Bjarnason, GA ;
Jordan, RCK ;
Sothern, RB .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 154 (02) :613-622