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Circadian Clock, Cell Cycle and Cancer

Circadian Rhythm and Cell Growth Regulation

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The Circadian Clock

Part of the book series: Protein Reviews ((PRON,volume 12))

Abstract

The circadian clock is a fundamental biological process that is pervasive in living organisms. Over the past decade, much has been learned about the molecular mechanism of the mammalian circadian clock. Studies have also led to the revelation of various connections between the circadian clock function and other basic biological processes, including the cell cycle and the DNA damage response. Several key regulators of circadian function have been identified to interact with regulators of DNA damage response pathways. In addition, expression of many key regulators of the cell cycle and the DNA damage response pathways display circadian rhythmic profiles, and these temporal expression profiles are altered in circadian clock deficient animals. Clinical studies have revealed deregulation of several core clock genes expression in different type of human cancers. Genetic studies from mice and Neurospora further suggest that the integration of the circadian clock with the cell division and the DNA damage response is very ancient. Understanding of the mechanistic details of how these basic processes are integrated and coordinated to achieve homeostasis will lead to new ideas for healthier life styles, and develop novel therapeutic strategies for many human disorders, including cancers.

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Abbreviations

AML:

Acute myeloid leukemia

APC:

Anaphase-promoting complex

ATM:

Ataxia telangiectasia mutated

ATR:

Ataxia telangiectasia Rad-3-related

ATRIP:

ATR interacting protein

Bmal1:

Brain and muscle ARNT-like 1 gene, also known as aryl hydrocarbon receptor nuclear translocator-like, Arntl

BRCA1:

Breast cancer 1

Chk1/2:

Checkpoint kinase 1/2

Cdk:

Cyclin dependent-kinases

Cry1:

Cryptochrome1 gene

DDR:

DNA damage response

DNA-PK:

DNA-dependent protein kinase

DSBs:

Double-strand breaks

Frq:

Frequency gene

G0 phase:

Quiescent cells stay in G0 phase, outside the cell cycle

G1 phase:

The first gap in the cell cycle

G2 phase:

The second gap in the cell cycle

HR:

Homologous recombination

IR:

Ionizing radiation

M phase:

The mitotic phase in the cell cycle

mPer2:

Mouse period2 gene

Npas2:

Neuronal PAS domain protein2, a paralogue of Clock gene

Rb:

Retinoblastoma gene

ROS:

Reactive oxygen species

S phase:

The DNA sysnthesis phase of the cell cycle

SCN:

Suprachiasmatic nuclei

SSBs:

Single-strand breaks

Tim:

Timeless gene

UV:

ultraviolet light

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Authors and Affiliations

  1. Department of Biochemistry and Molecular Biology, University of Texas Health Science Center at Houston, 6431 Fannin Street, MSB 6.200, Houston, TX, 7030, USA

    Zhaoyang Zhao & Cheng Chi Lee

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  1. Zhaoyang Zhao
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  2. Cheng Chi Lee
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Correspondence to Cheng Chi Lee .

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  1. Inst. Biochimie, Université de Fribourg, rue du Musee 5, Fribourg, 1700, Switzerland

    Urs Albrecht

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Zhao, Z., Lee, C.C. (2010). Circadian Clock, Cell Cycle and Cancer. In: Albrecht, U. (eds) The Circadian Clock. Protein Reviews, vol 12. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-1262-6_6

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