Cited by 175Circadian rhythm and melatoninCancer-related Molecular PathwaysCircular RNAs in diseases

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Circadian Clock, Cancer, and Chemotherapy

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Sancar, Aziz, Lindsey-Boltz, Laura A., Gaddameedhi, Shobhan, Selby, Christopher P., Ye, Rui, Chiou, Yi-Ying, Kemp, Michael G., Hu, Jinchuan, Lee, Jin Hyup, Ozturk, Nuri·2015·Biochemistry

DOI 10.1021/bi5007354PMC PMC4303322

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Abstract

The circadian clock is a global regulatory system that interfaces with most other regulatory systems and pathways in mammalian organisms. Investigations of the circadian clock–DNA damage response connections have revealed that nucleotide excision repair, DNA damage checkpoints, and apoptosis are appreciably influenced by the clock. Although several epidemiological studies in humans and a limited number of genetic studies in mouse model systems have indicated that clock disruption may predispose mammals to cancer, well-controlled genetic studies in mice have not supported the commonly held view that circadian clock disruption is a cancer risk factor. In fact, in the appropriate genetic background, clock disruption may instead aid in cancer regression by promoting intrinsic and extrinsic apoptosis. Finally, the clock may affect the efficacy of cancer treatment (chronochemotherapy) by modulating the pharmacokinetics and pharmacodynamics of chemotherapeutic drugs as well as the activity of the DNA repair enzymes that repair the DNA damage caused by anticancer drugs.

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Authors: Sancar, A., Lindsey-Boltz, L. A., Gaddameedhi, S., Selby, C. P., Ye, R., Chiou, Y.-Y., Kemp, M. G., Hu, J., Lee, J. H., & Ozturk, N.
Affiliations: University of North Carolina at Chapel Hill (US)
University of North Carolina School of Medicine , , , ,
Corresponding author: Sancar, Aziz
ORCID: Sancar, Aziz
Gaddameedhi, Shobhan
Selby, Christopher P.
Ye, Rui
Chiou, Yi-Ying
Kemp, Michael G.
Hu, Jinchuan
Lee, Jin Hyup
Venue: Biochemistry
Publisher: American Chemical Society (ACS)
Published: 2014-10-10
Volume: 54
Issue: 2
Pages: 110-123
ISSN: 0006-2960 (ISSN-L)
1520-4995
DOI: 10.1021/bi5007354
PMC: PMC4303322
OpenAlex: W2139669192
Cited by: 170
References: 105
Citations by year: 2026: 8 · 2025: 15 · 2024: 11 · 2023: 8 · 2022: 14 · 2021: 15 · 2020: 18 · 2019: 18 · 2018: 19 · 2017: 17 · 2016: 18 · 2015: 7 · 2014: 1
FWCI: 6.99
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: other-oa
pubs.acs.org/page/policy/authorchoice_termsofuse.html (vor, 365 d)
Locations: Biochemistry (publishedVersion, other-oa)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
UNC Libraries
Funders: National Institute of General Medical Sciences (GM31082, GM32833)
National Science Council Taiwan (NA)
Academia Sinica (NA)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Circular RNAs in diseases
Keywords: circadian clock, cancer, DNA damage response, nucleotide excision repair, DNA damage checkpoint, apoptosis, cancer risk, tumor regression, pharmacokinetics, pharmacodynamics, anticancer agents, DNA repair enzymes
MeSH terms: Animals, Antineoplastic Agents, DNA Damage, DNA Repair, Humans, Neoplasms, Risk Factors, Apoptosis, DNA Repair Enzymes, Drug Chronotherapy, Circadian Clocks

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