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Walker II. Jacob R. James C. Jennifer A. Randy J. Courtney DeVries. 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.
Light pollution and cancer
We describe the interrelation between core clock genes and the cell cycle, as courtney yates nude 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. Keywords: light at night; cancer; circadian rhythms; clock genes; cell cycle light at night ; cancer ; circadian rhythms ; clock genes ; cell cycle.
Introduction Overview of circadian rhythms: For the 3 to 4 billion years before electric light was invented, life on Earth evolved under the distinct pattern of light during the day and darkness at night.
Indeed, virtually all biological processes display rhythms of function that approximate 24 h [ 1 ]. Well-known examples of mammalian circadian rhythms are the sleep-wake cycle, body temperature, and patterns of hormone secretion e.
Importantly, several key processes involved in cancer are governed by circadian rhythms. For example, cell division shows strong daily cycles [ 2 ]. There courtney yates nude a bidirectional relationship between circadian rhythms and cell division. Disruption of circadian rhythms dramatically influences cell division and cancer development, whereas malignant transformation disrupts circadian organization [ 2 ]. Below, we present a brief review of the molecular circadian clock system and the importance of light during the day and darkness at night.
Then, we describe the role of circadian rhythms on the cell cycle, as well as the contribution of clock genes to oncogenesis. The suprachiasmatic nuclei SCN of the hypothalamus is the master circadian clock in mammals [ 4 ]: it is positioned at the top of a hierarchy of independent endogenous time-keepers. The cellular make-up of the SCN is diverse, and the SCN contains a variety of peptides and neurotransmitters [ 89 ]. As noted, the SCN serves as the master circadian clock at the top of a hierarchically organized system, however, circadian oscillators exist in virtually all tissues of multicellular organisms [ 10 ].
Tissue-specific clocks contain the molecular machinery necessary for self-sustaining rhythms [ 11 ] and have virtually the same molecular make-up as circadian oscillators in the SCN. Peripheral clocks are entrained to the external environment by the SCN via both neural and hormonal als, as well as through non-SCN als [ 12 ]. At a molecular level, the mammalian circadian system is driven by an autoregulatory feedback loop of transcriptional activators and repressors [ 1013 ].
This process requires about 24 h to complete a full cycle. In addition to the primary feedback loop, several additional regulatory loops influence the circadian clockwork, but the core clock components described above are protein products of clock genes that are essential for generation and regulation of circadian rhythms [ 18 ] Courtney yates nude of any of the core clock genes, Clock or Bmal1 [ 19 ], Per1 or Per2 [ 20 ], or Cry1 or Cry2 [ 21 ], disrupts circadian organization.
Several secondary and tertiary clock components have been identified as necessary for the generation of precise circadian rhythms [ 22 ], and the criteria for what constitutes core clock genes are continuously evolving. For example, RevErb and Per3 were not initially considered critical for maintaining circadian clock function; however, the importance of these genes for circadian regulation is now widely accepted [ 232425 ]. Light at night: Light is the most potent synchronizing factor for the SCN. In mammals, light information travels directly from intrinsically photosensitive melanopsin-containing retinal ganglion cells ipRGC in the eye through the retinohypothalamic tract to the SCN [ 26 ].
The SCN also receives indirect input from ipRGCs via the intergeniculate leaflet and input from rods and cones [ 272829 ]. Indeed, photo entrainment persists in melanopsin-deficient mice but not in triple knockouts that lack melanopsin, rod, and cone function [ 30 ]. Once light information reaches the SCN, it als via a multi-synaptic pathway to the pineal gland to regulate production and secretion of melatonin. Melatonin is secreted from the pineal gland at night in both nocturnal and diurnal animals. Circulating melatonin acts as a cue to entrain peripheral clocks via multiple interactions with the molecular clock mechanism, including phase-resetting clock genes [ 31 ].
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Thus, artificial light at night has the potential to substantially alter physiology and behavior via suppression of melatonin rhythms. At the molecular level, exposure to light rapidly induces Per1 [ 3536 ]. A pulse of light during the dark phase can phase advance or delay the circadian clock depending on the timing, duration, and intensity of the light al [ 3738 ]. The circadian system also appears to be sensitive to light intensities below the threshold that induces phase shifts e.
Exposure to dim light at night also influences the mammalian circadian system [ 4041 ].
Five lux of nighttime light exposure is comparable to levels of light pollution found in urban areas [ 4647 ] and sleeping environments [ 4849 ]. Exposure to chronic low levels of light at night alters circadian clock genes in both the SCN and peripheral tissues in mice and insects [ 505152 ]. Furthermore, expression of Bmal1Per1Per2Cry1Cry2and Rev-Erb are all repressed in the liver by exposure to dim light at night [ 50 ]. Nocturnal light may affect the liver through both autonomic and hormonal pathways [ 53 ]. Similar changes in circadian clock function are also apparent in the SCN of Siberian hamsters Phodopus sungorus exposed to dim light at night [ 54 ].
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Importantly, rodents are typically more sensitive to lower-intensity lighting than humans [ 3255 ]. However, light at night exposure also influences human circadian rhythms. The sleep patterns of people exposed to only natural light outdoor camping were more closely synchronized to solar time compared to individuals with exposure to light at night [ 56 ]. Furthermore, exposure to natural lighting reduced individual variability in melatonin and sleep rhythms, making late chronotypes more similar to early chronotypes [ 56 ].
In normally proliferating mammalian cells, the rhythmic circadian clock and cell cycles are phase-locked [ 57 ]. The coupling of these two cycles remains an area of active research, however, several shared regulatory mechanisms highlight the molecular underpinnings of this coupling.
First, it is important to understand how the cell cycle can regulate the circadian cycle, and vice versa.
Circadian clock regulation of the cell cycle generally occurs via interaction at the transcriptional or protein level between molecular circadian clock elements and [ 1 ] the cyclin-cyclin-dependent kinase CDK complexes and [ 2 ] the cell cycle inhibitors that regulate gating of the unidirectional progression through the stages of the cell cycle [ 58 ].
Taken together, transitions through all the stages of the cell cycle are under the control of the circadian clock.
Conversely, evidence of cell cycle regulation of the circadian clock and rhythmicity is much more sparse, but compelling none the less, especially in the context of cancer. DNA damage can reset the circadian clock [ 6465 ], which is potentially mediated by Cryptochrome [ 66 ]. In addition to reciprocal regulation between cyclic pathways, common enzymatic regulators in the phosphorylation and ubiquitination pathways are shared between the circadian clock and cell cycle pathways.
These post-transcriptional modifiers could serve as both coupling and common regulatory mechanisms. Additionally, phosphorylation via AMPK in stabilization of the cell cycle p27 protein [ 79 ], whereas the circadian clock protein CRY1 is destabilized [ 80 ].
Taken together, rhythms in the cell cycle and the circadian clock are normally coupled together, can reciprocally regulate each other, and have both shared and opposing effects by post-transcriptional modifiers. Dysregulation in the shared regulatory and coupling connections between the two pathways can be both necessary and sufficient for tumorigenesis. Because of the reciprocal regulation of core clock genes CCG and the cell cycle, it is not surprising that numerous studies establish an association between CCG and oncogenesis.
Indeed, studies demonstrate a relationship between CCG and multiple cancer types, including breast, colorectal, endometrial, lung, prostate, pancreatic, and multiple lymphomas and leukemias [ 8182 ]. Breast cancer patients frequently display mutations and increased methylation of the gene promoters in PER 1 and 2 [ 838485 ]. Reduced expression of PERs and CRYs within breast tumors relative to surrounding normal breast tissue have also been reported [ 86878889 ].
Similarly, reductions in the expression of one or more PERs are seen in patient samples of colorectal, prostate, adrenal, ovarian, endometrial, lung, glioma, and pancreatic tumors [ 83909192939495 ]. In contrast, studies examining PER 2 expression in patient samples of gastric cancer report conflicting .