Night shift schedule causes circadian dysregulation of DNA repair genes and elevated DNA damage in humans

Koritala, Bala S. C.; Porter, Kenneth I.; Arshad, Osama A.; Gajula, Rajendra P.; Mitchell, Hugh D.; Arman, Tarana; Manjanatha, Mugimane G.; Teeguarden, Justin G.; Dongen, Hans P A Van; McDermott, Jason; Gaddameedhi, Shobhan

doi:10.1111/jpi.12726

Cited by 60 publications

(58 citation statements)

References 67 publications

(157 reference statements)

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“…Ideally, to properly assess a circadian oscillation (for instance, in activity, melatonin oscillation, or mRNA oscillation), a researcher conducts serial measurements in 2–4 h increments across several days, and then tests for oscillations in these time-series data. Indeed, this technique is quite feasible with serial sampling of human blood from volunteers, and has revealed that night shift work may be a risk factor for DNA damage that can lead to cancer [ 170 , 171 ]. However, serial sampling of most solid tumors is impossible due to ethical and practical considerations.…”

Section: Clinical Applications: Myc Inhibition and Measurement Of The Molecular Clock In Patientsmentioning

confidence: 99%

MYC Ran Up the Clock: The Complex Interplay between MYC and the Molecular Circadian Clock in Cancer

Burchett

Clark

Altman

2021

IJMS

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The MYC oncoprotein and its family members N-MYC and L-MYC are known to drive a wide variety of human cancers. Emerging evidence suggests that MYC has a bi-directional relationship with the molecular clock in cancer. The molecular clock is responsible for circadian (~24 h) rhythms in most eukaryotic cells and organisms, as a mechanism to adapt to light/dark cycles. Disruption of human circadian rhythms, such as through shift work, may serve as a risk factor for cancer, but connections with oncogenic drivers such as MYC were previously not well understood. In this review, we examine recent evidence that MYC in cancer cells can disrupt the molecular clock; and conversely, that molecular clock disruption in cancer can deregulate and elevate MYC. Since MYC and the molecular clock control many of the same processes, we then consider competition between MYC and the molecular clock in several select aspects of tumor biology, including chromatin state, global transcriptional profile, metabolic rewiring, and immune infiltrate in the tumor. Finally, we discuss how the molecular clock can be monitored or diagnosed in human tumors, and how MYC inhibition could potentially restore molecular clock function. Further study of the relationship between the molecular clock and MYC in cancer may reveal previously unsuspected vulnerabilities which could lead to new treatment strategies.

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Section: Clinical Applications: Myc Inhibition and Measurement Of The Molecular Clock In Patientsmentioning

confidence: 99%

MYC Ran Up the Clock: The Complex Interplay between MYC and the Molecular Circadian Clock in Cancer

Burchett

Clark

Altman

2021

IJMS

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“…However, inflammation can also induce other metabolic, immunosuppressive, and epigenetic changes that are also key to cancer progression. Other food or lifestyle carcinogens identified by IARC such as red meat, wood dust, hot beverages, night shift work, oral contraceptives, and post-menopausal estrogen therapy appear to cause cancer through inflammation, irritation, disrupted circadian rhythm, or chemical activation of cell growth pathways [81][82][83].…”

Section: Cancer As An Environmental Disease (The Exposome View)mentioning

confidence: 99%

Metabolomics and the Multi-Omics View of Cancer

Wishart

2022

Metabolites

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Cancer is widely regarded to be a genetic disease. Indeed, over the past five decades, the genomic perspective on cancer has come to almost completely dominate the field. However, this genome-only view is incomplete and tends to portray cancer as a disease that is highly heritable, driven by hundreds of complex genetic interactions and, consequently, difficult to prevent or treat. New evidence suggests that cancer is not as heritable or purely genetic as once thought and that it really is a multi-omics disease. As highlighted in this review, the genome, the exposome, and the metabolome all play roles in cancer’s development and manifestation. The data presented here show that >90% of cancers are initiated by environmental exposures (the exposome) which lead to cancer-inducing genetic changes. The resulting genetic changes are, then, propagated through the altered DNA of the proliferating cancer cells (the genome). Finally, the dividing cancer cells are nourished and sustained by genetically reprogrammed, cancer-specific metabolism (the metabolome). As shown in this review, all three “omes” play roles in initiating cancer. Likewise, all three “omes” interact closely, often providing feedback to each other to sustain or enhance tumor development. Thanks to metabolomics, these multi-omics feedback loops are now much more evident and their roles in explaining the hallmarks of cancer are much better understood. Importantly, this more holistic, multi-omics view portrays cancer as a disease that is much more preventable, easier to understand, and potentially, far more treatable.

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“…Moreover, environmental or physiological perturbation of circadian rhythms such as shift work, abnormal sleep timing, irregular psychosociological stresses, and illness, can cause interindividual variability in both cancer growth and the response to cancer therapy (Y. Lee et al, 2019a;Walker et al, 2020a;Koritala et al, 2021). Circadian disruption may also be related to the chronic sleep loss and depression suffered by many cancer patients following diagnosis and treatment (Innominato et al, 2014;Telias and Wilcox, 2019).…”

Section: Circadian Regulation Of the Tumor Cell Cycle Can Affectmentioning

confidence: 99%

Circadian Rhythms, Disease and Chronotherapy

2021

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Circadian clocks are biological timing mechanisms that generate 24-h rhythms of physiology and behavior, exemplified by cycles of sleep/wake, hormone release, and metabolism. The adaptive value of clocks is evident when internal body clocks and daily environmental cycles are mismatched, such as in the case of shift work and jet lag or even mistimed eating, all of which are associated with physiological disruption and disease. Studies with animal and human models have also unraveled an important role of functional circadian clocks in modulating cellular and organismal responses to physiological cues (ex., food intake, exercise), pathological insults (e.g. virus and parasite infections), and medical interventions (e.g. medication). With growing knowledge of the molecular and cellular mechanisms underlying circadian physiology and pathophysiology, it is becoming possible to target circadian rhythms for disease prevention and treatment. In this review, we discuss recent advances in circadian research and the potential for therapeutic applications that take patient circadian rhythms into account in treating disease.

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Night shift schedule causes circadian dysregulation of DNA repair genes and elevated DNA damage in humans

Abstract: jointly supervised the work (joint senior authorship).

Cited by 60 publications

References 67 publications

MYC Ran Up the Clock: The Complex Interplay between MYC and the Molecular Circadian Clock in Cancer

MYC Ran Up the Clock: The Complex Interplay between MYC and the Molecular Circadian Clock in Cancer

Metabolomics and the Multi-Omics View of Cancer

Circadian Rhythms, Disease and Chronotherapy

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