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      Light Pollution and Cancer

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          Abstract

          For many individuals in industrialized nations, the widespread adoption of electric lighting has dramatically affected the circadian organization of physiology and behavior. Although initially assumed to be innocuous, exposure to artificial light at night (ALAN) is associated with several disorders, including increased incidence of cancer, metabolic disorders, and mood disorders. Within this review, we present a brief overview of the molecular circadian clock system and the importance of maintaining fidelity to bright days and dark nights. We describe the interrelation between core clock genes and the cell cycle, as well as the contribution of clock genes to oncogenesis. Next, we review the clinical implications of disrupted circadian rhythms on cancer, followed by a section on the foundational science literature on the effects of light at night and cancer. Finally, we provide some strategies for mitigation of disrupted circadian rhythms to improve health.

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          Molecular components of the mammalian circadian clock.

          Caroline Ko, Joseph S Takahashi (2006)
          Circadian rhythms are approximately 24-h oscillations in behavior and physiology, which are internally generated and function to anticipate the environmental changes associated with the solar day. A conserved transcriptional-translational autoregulatory loop generates molecular oscillations of 'clock genes' at the cellular level. In mammals, the circadian system is organized in a hierarchical manner, in which a master pacemaker in the suprachiasmatic nucleus (SCN) regulates downstream oscillators in peripheral tissues. Recent findings have revealed that the clock is cell-autonomous and self-sustained not only in a central pacemaker, the SCN, but also in peripheral tissues and in dissociated cultured cells. It is becoming evident that specific contribution of each clock component and interactions among the components vary in a tissue-specific manner. Here, we review the general mechanisms of the circadian clockwork, describe recent findings that elucidate tissue-specific expression patterns of the clock genes and address the importance of circadian regulation in peripheral tissues for an organism's overall well-being.
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            Regulation of Circadian Behavior and Metabolism by Rev-erbα and Rev-erbβ

            Han-keun Cho, Xuan Zhao, Megumi Hatori … (2012)
            The circadian clock acts at the genomic level to coordinate internal behavioral and physiologic rhythms via the CLOCK-BMAL transcriptional heterodimer. Although the nuclear receptors REV-ERBα and β have been proposed to form an accessory feedback loop that contributes to clock function 1,2 , their precise roles and importance remain unresolved. To establish their regulatory potential we generated comparative cistromes of both REV-ERB isoforms, which revealed shared recognition at over 50% of their total sites and extensive overlap with the master circadian regulator BMAL1. While Rev-erbα has been shown to directly regulate Bmal1 expression 1,2 , the cistromic analysis reveals a direct connection between Bmal1 and Rev-erbα and β regulatory circuits than previously suspected. Genes within the intersection of the BMAL1, REV-ERBα and REV-ERBβ cistromes are highly enriched for both clock and metabolic functions. As predicted by the cistromic analysis, dual depletion of Rev-erbα/β function by creating double-knockout mice (DKOs) profoundly disrupted circadian expression of core circadian clock and lipid homeostatic gene networks. As a result, DKOs show strikingly altered circadian wheel-running behavior and deregulated lipid metabolism. These data now ally Rev-erbα/β with Per, Cry and other components of the principal feedback loop that drives circadian expression and suggest a more integral mechanism for the coordination of circadian rhythm and metabolism.
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              Role of the CLOCK protein in the mammalian circadian mechanism.

              N Gekakis, D Staknis, H B Nguyen … (1998)
              The mouse Clock gene encodes a bHLH-PAS protein that regulates circadian rhythms and is related to transcription factors that act as heterodimers. Potential partners of CLOCK were isolated in a two-hybrid screen, and one, BMAL1, was coexpressed with CLOCK and PER1 at known circadian clock sites in brain and retina. CLOCK-BMAL1 heterodimers activated transcription from E-box elements, a type of transcription factor-binding site, found adjacent to the mouse per1 gene and from an identical E-box known to be important for per gene expression in Drosophila. Mutant CLOCK from the dominant-negative Clock allele and BMAL1 formed heterodimers that bound DNA but failed to activate transcription. Thus, CLOCK-BMAL1 heterodimers appear to drive the positive component of per transcriptional oscillations, which are thought to underlie circadian rhythmicity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 08 December 2020
                Publication date Collection: December 2020
                Volume: 21
                Issue: 24
                Electronic Location Identifier: 9360
                Affiliations
                [1 ]Department of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV 26506, USA; jrbumgarner@ 123456mix.wvu.edu (J.R.B.); james.walton@ 123456hsc.wvu.edu (J.C.W.); jal0075@ 123456mix.wvu.edu (J.A.L.); ohm0001@ 123456mix.wvu.edu (O.H.M.-F.); randy.nelson@ 123456hsc.wvu.edu (R.J.N.); courtney.devries@ 123456hsc.wvu.edu (A.C.D.)
                [2 ]Department of Medicine, Division of Oncology/Hematology, West Virginia University, Morgantown, WV 26506, USA
                [3 ]West Virginia University Cancer Institute, West Virginia University, Morgantown, WV 26506, USA
                Author notes
                Author information
                https://orcid.org/0000-0001-6209-5015
                https://orcid.org/0000-0002-0387-9263
                https://orcid.org/0000-0002-3049-1029
                https://orcid.org/0000-0002-8194-4016
                Article
                Publisher ID: ijms-21-09360
                DOI: 10.3390/ijms21249360
                PMC ID: 7764771
                PubMed ID: 33302582
                SO-VID: f5fa4038-edd2-4c35-90d1-cb0f2fdaa1b1
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 24 November 2020
                Date accepted : 06 December 2020
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: light at night,cancer,circadian rhythms,clock genes,cell cycle
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: light at night, cancer, circadian rhythms, clock genes, cell cycle

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