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Effects of Light and Food Schedules on Liver and Tumor Molecular Clocks in Mice
Open accessAbstract
BACKGROUND: Disrupted circadian coordination accelerates malignant growth, but the molecular mechanism is unclear. METHODS: Healthy or Glasgow osteosarcoma-bearing mice (n = 162) were synchronized with light and darkness over 2-3 weeks, submitted to an 8-hour advance onset of light every 2 days (chronic jet lag) to disrupt circadian coordination, or submitted to chronic jet lag and meal timing to prevent molecular clock alteration. The expression of molecular clock genes and of the cell cycle genes c-Myc and p53 in liver and tumor was determined with quantitative reverse transcription-polymerase chain reaction at six circadian times over a 24-hour period of light and darkness and analyzed with analysis of variance and cosinor. Tumor weight was measured daily over the course of the experiment. All statistical tests were two-sided. RESULTS: In synchronized mice, mean mRNA levels of clock genes Rev-erbalpha, Per2, and Bmal1 varied by 206-, four-, and 26-fold, respectively, over the 24 hours in healthy mouse liver; by 36-, 35-, and 32-fold in the livers of tumor-bearing mice; and by 9.4-, 5.5-, and sixfold in tumor tissue (P = .046 to <.001). In mice subjected to chronic jet lag, the periodic changes were dampened and the clock gene rhythms were temporally shifted in liver and ablated in tumor, and tumor growth was accelerated. Meal timing reversed the chronic jet lag-induced alterations in Rev-erbalpha and Per2 expression in liver and of all three clock genes in tumor and slowed tumor growth. Tumor growth differed as a function of light and feeding schedules (P = .04). No obvious rhythm was detected for p53 or c-Myc in liver or tumor tissues of synchronized mice. In healthy mice subjected to chronic jet lag, the mean level of p53 expression was cut in half (P = .002), and a 12-fold circadian variation in c-Myc mRNA level (P = .03) was induced in the liver of healthy mice, whereas complex expression patterns were found in the liver and tumor of tumor-bearing mice. CONCLUSIONS: Altered light-dark or feeding schedules modified the expression of molecular clock genes and genes involved in carcinogenesis and tumor progression.
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“this protocol has been shown to disrupt the oscillations of the core circadian genes in multiple tissues (Filipski et al., 2005; Lee et al., 2010; Thaiss et al., 2014).”
From Circadian Rhythm Disruption Promotes Lung Tumorigenesis (2016) · cites this paper as Filipski et al., 2005
In the citing paper
“Emerging evidence in several different cellular and in vivo models points to an important role of the core circadian genes in carcinogenesis (Filipski et al., 2005; Fu et al., 2002; Gery et al., 2006; Janich et al., 2011; Kettner et al., 2014; Lee et al., 2010; Puram et al., 2016; Sahar and Sassone-Corsi, 2009; Van Dycke et al., 2015; Wood et al., 2008).”
From Circadian Rhythm Disruption Promotes Lung Tumorigenesis (2016) · cites this paper as Filipski et al., 2005
In the citing paper
“Earlier reports using germline mutations in circadian components have highlighted a role for circadian rhythm disruption in tumor predisposition (Filipski et al., 2005; Fu et al., 2002; Gery et al., 2006; Janich et al., 2011; Kettner et al., 2014; Lee et al., 2010; Sahar and Sassone-Corsi, 2009; Van Dycke et al., 2015; Wood et al., 2008).”
From Circadian Rhythm Disruption Promotes Lung Tumorigenesis (2016) · cites this paper as Filipski et al., 2005
In the citing paper
“This would be in line with other studies in which phase advances induce c-myc expression directly and 3 days after exposure [11, 27”
From Chronically Alternating Light Cycles Increase Breast Cancer Risk in Mice (2015) · cites this paper as [11]
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Self-citation
Metadata
- Authors
- Filipski, E., Innominato, P. F., Wu, M., Li, X.-M., Iacobelli, S., Xian, L.-J., & Levi, F.
- Affiliations
- Inserm (FR)
- Corresponding author
- Filipski, E.
- Venue
- JNCI Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-04-05
- Volume
- 97
- Issue
- 7
- Pages
- 507-517
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2128032039
- Cited by
- 200
- References
- 48
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 4 · 2023: 6 · 2022: 6 · 2021: 7 · 2020: 10 · 2019: 6 · 2018: 10 · 2017: 9 · 2016: 14 · 2015: 9 · 2014: 13 · 2013: 12 · 2012: 12
- FWCI
- 5.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JNCI Journal of the National Cancer Institute (publishedVersion)
- PubMed (publishedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Zenodo (CERN European Organization for Nuclear Research) (other-oa)
- 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 › Physiology (medical) › Dietary Effects on Health
- Keywords
- circadian rhythm, jet lag, light-dark cycle, meal timing, feeding schedule, clock genes, NR1D1, Per2, Bmal1, osteosarcoma, liver, tumor growth, p53, c-Myc, carcinogenesis, tumor progression, molecular clock
- MeSH terms
- Analysis of Variance, Animals, Circadian Rhythm, DNA-Binding Proteins, Food, Light, Liver, Male, Nuclear Proteins, RNA, Messenger, Transcription Factors, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Proto-Oncogene Proteins c-myc, Receptors, Cytoplasmic and Nuclear, Cell Cycle Proteins, Reverse Transcriptase Polymerase Chain Reaction, Mice, Period Circadian Proteins, Nuclear Receptor Subfamily 1, Group D, Member 1
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