Circadian gene variants in cancer
Open accessAbstract
Humans as diurnal beings are active during the day and rest at night. This daily oscillation of behavior and physiology is driven by an endogenous circadian clock not environmental cues. In modern societies, changes in lifestyle have led to a frequent disruption of the endogenous circadian homeostasis leading to increased risk of various diseases including cancer. The clock is operated by the feedback loops of circadian genes and controls daily physiology by coupling cell proliferation and metabolism, DNA damage repair, and apoptosis in peripheral tissues with physical activity, energy homeostasis, immune and neuroendocrine functions at the organismal level. Recent studies have revealed that defects in circadian genes due to targeted gene ablation in animal models or single nucleotide polymorphism, deletion, deregulation and/or epigenetic silencing in humans are closely associated with increased risk of cancer. In addition, disruption of circadian rhythm can disrupt the molecular clock in peripheral tissues in the absence of circadian gene mutations. Circadian disruption has recently been recognized as an independent cancer risk factor. Further study of the mechanism of clock-controlled tumor suppression will have a significant impact on human health by improving the efficiencies of cancer prevention and treatment.
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Germline or tissue-specific ablation of core circadian genes promotes genomic instability and accelerates tumorigenesis and cancer progression in mice.
“Recent studies have revealed that germline or tissue-specific ablation of core circadian genes promotes genomic instability and accelerates both tumorigenesis and cancer progression in mice (Kettner et al., 2014)”
From Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis (2016) · cites this paper as Kettner et al., 2014
Mouse models with germline or tissue-specific ablation of circadian genes show increased risk of genomic instability, neoplastic growth, and cancer.
“Although mouse models with germline or tissue-specific ablation of circadian genes display increased risk of genomic instability, neoplastic growth and cancer (Kettner et al., 2014)”
From Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis (2016) · cites this paper as Kettner et al., 2014
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References 310 · Cited by 147
- Authors
- Kettner, N. M., Katchy, C. A., & Fu, L.
- Affiliations
- Agricultural Research Service (US)
- Baylor College of Medicine (US)
- Corresponding author
- Fu, Loning
- Venue
- Annals of Medicine
- Publisher
- Informa UK Limited
- Published
- 2014-06
- Volume
- 46
- Issue
- 4
- Pages
- 208-220
- ISSN
- 0785-3890 (ISSN-L)
- 1365-2060
- PMC
- PMC4153443
- OpenAlex
- W2035042010
- Cited by
- 147
- References
- 310
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 23 · 2023: 12 · 2022: 11 · 2021: 17 · 2020: 12 · 2019: 13 · 2018: 13 · 2017: 12 · 2016: 15 · 2015: 7 · 2014: 1 · 2013: 1
- FWCI
- 1.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Agriculture
- National Institutes of Health
- Agricultural Research Service
- National Cancer Institute (R01CA137019, R01 CA137019-01A)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK056338)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Keywords
- circadian clock, circadian genes, cancer risk, circadian rhythm disruption, single nucleotide polymorphisms, gene ablation, epigenetic silencing, DNA repair, apoptosis, cancer prevention
- MeSH terms
- Animals, Circadian Rhythm, Homeostasis, Humans, Mutation, Neoplasms, Risk Factors, Genetic Variation, Circadian Clocks
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