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Circadian disruption accelerates liver carcinogenesis in mice
Elisabeth Filipski1, Perumal Subramanian, Jennyfer Carrière
1INSERM, U776 Rythmes Biologiques et Cancers, Hôpital Paul Brousse, Villejuif F-94807, France.
Mutation Research
|October 17, 2009
Summary
Chronic jet-lag (CJL) combined with the carcinogen diethylnitrosamine (DEN) significantly promoted liver cancer in mice. Circadian disruption prolonged DEN
Area of Science:
- Chronobiology
- Hepatocarcinogenesis
- Cancer Promotion
Background:
- The circadian timing system regulates daily physiological processes, and disruption (e.g., shift work) is linked to cancer risk.
- Chronic jet-lag (CJL) in mice alters clock gene expression and promotes tumor growth.
- This study investigates CJL's role in promoting liver cancer induced by diethylnitrosamine (DEN).
Purpose of the Study:
- To investigate the role of chronic jet-lag (CJL) as a tumor promoter in mice exposed to the hepatic carcinogen diethylnitrosamine (DEN).
Main Methods:
- Mice received DEN (10 mg/kg/day) and were randomized to either a standard light-dark cycle (LD 12:12) or CJL.
- Rest-activity, body temperature, and serum liver enzymes were monitored.
- Neoplastic lesions were assessed at 10 months.
Main Results:
- DEN induced liver cancers in all mice.
- CJL significantly increased liver tumors and aspartate aminotransferase levels compared to LD mice.
- CJL also led to larger tumors and a greater diversity of tumor types.
Conclusions:
- Circadian disruption, particularly from CJL, actively promotes liver carcinogenesis initiated by DEN.
- Maintaining circadian coordination is crucial for potentially slowing or reversing cancer development post-carcinogen exposure.
