Circadian disruption in mice through chronic jet lag-like conditions modulates molecular profiles of cancer in nucleus accumbens and prefrontal cortex.

Publisher: Irl Press At Oxford University Press Country of Publication: England NLM ID: 8008055 Publication Model: Print Cited Medium: Internet ISSN: 1460-2180 (Electronic) Linking ISSN: 01433334 NLM ISO Abbreviation: Carcinogenesis Subsets: MEDLINE

Publication: Oxford : Irl Press At Oxford University Press
Original Publication: [New York, IRL Press]

Gene Expression Regulation, Neoplastic* ; Photoperiod*; Biomarkers, Tumor/*metabolism ; Brain Neoplasms/*pathology ; Jet Lag Syndrome/*complications ; Nucleus Accumbens/*pathology ; Prefrontal Cortex/*pathology; Animals ; Biomarkers, Tumor/genetics ; Brain Neoplasms/etiology ; Brain Neoplasms/metabolism ; Chronic Disease ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Nucleus Accumbens/metabolism ; Prefrontal Cortex/metabolism ; RNA-Seq

Biological rhythms regulate physiological activities. Shiftwork disrupts normal circadian rhythms and may increase the risk of cancer through unknown mechanisms. To mimic environmental light/dark changes encountered by shift workers, a protocol called 'chronic jet lag (CJL)' induced by repeatedly shifting light-dark cycles has been used. Here, we subjected mice to CJL by advancing light-dark cycle by 6 h every 2 days, and conducted RNA sequencing to analyze the expression profile and molecular signature in the brain areas of prefrontal cortex and nucleus accumbens. We also performed positron emission tomography (PET) imaging to monitor changes related to glucose metabolism in brain. Our results reveal systematic reprogramming of gene expression associated with cancer-related pathways and metabolic pathways in prefrontal cortex and nucleus accumbens. PET imaging indicates that glucose uptake level was significantly reduced in whole brain as well as the individual brain regions. Moreover, qPCR analysis describes that the expression levels of cancer-related genes were altered in prefrontal cortex and nucleus accumbens. Overall, these results suggest a molecular and metabolic link with CJL-mediated cancer risk, and generate hypotheses on how CJL increases the susceptibility to cancer.
(© The Author(s) 2021. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

0 (Biomarkers, Tumor)

Date Created: 20210220 Date Completed: 20211122 Latest Revision: 20211122

20231215

10.1093/carcin/bgab012

33608694