Cited by 125Circadian rhythm and melatoninSleep and Work-Related FatigueCancer, Stress, Anesthesia, and Immune Response

Circadian disruption in experimental cancer processes

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Filipski, Elisabeth, Lévi, Francis·2009·Integrative Cancer Therapies

Abstract

The circadian timing system (CTS) coordinated by the suprachiasmatic nuclei (SCN) of the hypothalamus regulates daily rhythms of behavior, physiology, as well as cellular metabolism and proliferation. Altered circadian rhythms predict for poor survival in cancer patients. An increased incidence of several cancers has been reported in flight attendants and in shift workers. To explore the contribution of the CTS to tumor growth, we developed experimental models of disrupted or enhanced circadian coordination through stereotaxic destruction of the SCN, modifications of photoperiodic or feeding synchronizers and/or the administration of pharmacologic agents. SCN ablation or exposure to experimental chronic jetlag (CJL, consisting of an 8-hour advance of the light-dark cycle every 2 days) caused alterations in circadian physiology and significantly accelerated tumor growth. CJL suppressed or altered the rhythms of clock gene and cell cycle gene expression in mouse liver. It increased p53 and decreased c-Myc expression, a result in line with the promotion of diethylnitrosamine -initiated hepatocarcinogenesis in jet-lagged mice. The accelerating effect of CJL on tumor growth was counterbalanced by the regular timing of food access over the 24-h. Meal timing prevented the circadian disruption produced by CJL and slowed down tumor growth. In synchronized mice, meal timing reinforced host circadian coordination, phase-shifted the transcriptional rhythms of clock genes in the liver of tumor-bearing mice and slowed down cancer progression. These results support the role of the CTS in cancer progression and call for the development of therapeutic strategies aimed at preventing or treating circadian clock dysfunctions.

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Crossref · 10.1177/1534735409352085

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Authors
Filipski, E., & Lévi, F.
Affiliations
  • Université Paris-Sud (FR)
  • Hôpital Paul Brousse, Villejuif, France, Université Paris-Sud, Orsay, France
Corresponding author
Filipski, Elisabeth
Venue
Integrative Cancer Therapies
Published
2009-12
Volume
8
Issue
4
Pages
298-302
ISSN
  • 1534-7354 (ISSN-L)
  • 1552-695X
OpenAlex
W2036196597
Cited by
125
References
38
Citations by year
2026: 3 · 2025: 5 · 2024: 9 · 2023: 3 · 2022: 7 · 2021: 10 · 2020: 7 · 2019: 5 · 2018: 8 · 2017: 7 · 2016: 4 · 2015: 10 · 2014: 13 · 2013: 15 · 2012: 8
FWCI
2.69
Type
journal article
Language
en
Open access
Locations
  • Integrative Cancer Therapies (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
Keywords
circadian rhythm, circadian clock, suprachiasmatic nucleus, circadian rhythm disruption, tumor growth, jet lag, meal timing, photoperiod, clock genes, p53, c-Myc, hepatocarcinogenesis, diethylnitrosamine, liver cancer, shift work, tumor progression
MeSH terms
Animals, Chronic Disease, Circadian Rhythm, Disease Models, Animal, Food, Male, Neoplasms, Experimental, Suprachiasmatic Nucleus, Photoperiod, Disease Progression, Jet Lag Syndrome, Mice

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