Crosstalk between Circadian Rhythm and Diseases

A special issue of Clocks & Sleep (ISSN 2624-5175). This special issue belongs to the section "Disorders".

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 10721

Special Issue Editor


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Guest Editor
Department of Diagnostic Pathology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho, Sunto-gun, Shizuoka Prefecture 411-8777, Japan
Interests: crosstalk between circadian rhythm and tumor progression; pathological analysis in human and mouse tissues; functional analysis of DEC1 and DEC2 in tumor progression; molecular pathways of DEC1 and DEC2; crosstalk between basic and clinical research, involving clock genes
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Special Issue Information

Dear Colleagues,

Circadian rhythm is dominantly regulated by clock genes. Recent evidence suggests that the clock genes CLOCK, BMAL1/2, DEC1/2, PER1/2/3, and CRY1/2 play important roles in tumor progression, metabolism, immune responses, and sleep disorders by regulating apoptosis-related factors, cell cycle regulators, and inflammatory factors. On the other hand, various kinds of stress, such as hypoxia, inflammation, and anti-tumor drugs, affect the expression of clock genes. Therefore, clock genes have multiple functions in vivo that are associated with various kinds of diseases. Our aim is to improve the understanding of crosstalk between circadian rhythms, clock genes, and diseases to allow the development of strategies to overcome diseases, involving clock gene abnormalities. We encourage the submission of original articles and reviews involving circadian rhythm/clock genes and diseases.

Topics include, but are not limited to the following:

  • Relevant circadian rhythm/clock genes and diseases
  • Molecular pathways of clock genes, involving tumor progression, metabolism, inflammation, etc.
  • Functional analyses of clock genes in mouse models

The conjunct Special Issue in IJMS: Crosstalk between Circadian Rhythm and Diseases

Dr. Fuyuki Sato
Guest Editor

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Keywords

  • circadian rhythm
  • clock genes
  • tumor progression
  • metabolism
  • immune response
  • inflammation
  • molecular pathway

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Published Papers (2 papers)

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Research

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13 pages, 3948 KiB  
Article
Potential Role of DEC1 in Cervical Cancer Cells Involving Overexpression and Apoptosis
by Fuyuki Sato, Ujjal K. Bhawal, Nao Sugiyama, Shoko Osaki, Kosuke Oikawa and Yasuteru Muragaki
Clocks & Sleep 2020, 2(1), 26-38; https://doi.org/10.3390/clockssleep2010004 - 26 Jan 2020
Cited by 5 | Viewed by 3435
Abstract
Basic helix-loop-helix (BHLH) transcription factors differentiated embryonic chondrocyte gene 1 (DEC1) and gene 2 (DEC2) regulate circadian rhythms, apoptosis, epithelial mesenchymal transition (EMT), invasions and metastases in various kinds of cancer. The stem cell markers SOX2 and c-MYC are involved in the regulation [...] Read more.
Basic helix-loop-helix (BHLH) transcription factors differentiated embryonic chondrocyte gene 1 (DEC1) and gene 2 (DEC2) regulate circadian rhythms, apoptosis, epithelial mesenchymal transition (EMT), invasions and metastases in various kinds of cancer. The stem cell markers SOX2 and c-MYC are involved in the regulation of apoptosis and poor prognosis. In cervical cancer, however, their roles are not well elucidated yet. To determine the function of these genes in human cervical cancer, we examined the expression of DEC1, DEC2, SOX2 and c-MYC in human cervical cancer tissues. In immunohistochemistry, they were strongly expressed in cancer cells compared with in non-cancerous cells. Notably, the strong rate of DEC1 and SOX2 expressions were over 80% among 20 cases. We further examined the roles of DEC1 and DEC2 in apoptosis. Human cervical cancer HeLa and SiHa cells were treated with cisplatin—HeLa cells were sensitive to apoptosis, but SiHa cells were resistant. DEC1 expression decreased in the cisplatin-treated HeLa cells, but had little effect on SiHa cells. Combination treatment of DEC1 overexpression and cisplatin inhibited apoptosis and affected SOX2 and c-MYC expressions in HeLa cells. Meanwhile, DEC2 overexpression had little effect on apoptosis and on SOX2 and c-MYC expressions. We conclude that DEC1 has anti-apoptotic effects and regulates SOX2 and c-MYC expressions on apoptosis. Full article
(This article belongs to the Special Issue Crosstalk between Circadian Rhythm and Diseases)
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Review

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26 pages, 1165 KiB  
Review
MicroRNA: A Key Player for the Interplay of Circadian Rhythm Abnormalities, Sleep Disorders and Neurodegenerative Diseases
by Chisato Kinoshita, Yayoi Okamoto, Koji Aoyama and Toshio Nakaki
Clocks & Sleep 2020, 2(3), 282-307; https://doi.org/10.3390/clockssleep2030022 - 23 Jul 2020
Cited by 29 | Viewed by 6836
Abstract
Circadian rhythms are endogenous 24-h oscillators that regulate the sleep/wake cycles and the timing of biological systems to optimize physiology and behavior for the environmental day/night cycles. The systems are basically generated by transcription–translation feedback loops combined with post-transcriptional and post-translational modification. Recently, [...] Read more.
Circadian rhythms are endogenous 24-h oscillators that regulate the sleep/wake cycles and the timing of biological systems to optimize physiology and behavior for the environmental day/night cycles. The systems are basically generated by transcription–translation feedback loops combined with post-transcriptional and post-translational modification. Recently, evidence is emerging that additional non-coding RNA-based mechanisms are also required to maintain proper clock function. MicroRNA is an especially important factor that plays critical roles in regulating circadian rhythm as well as many other physiological functions. Circadian misalignment not only disturbs the sleep/wake cycle and rhythmic physiological activity but also contributes to the development of various diseases, such as sleep disorders and neurodegenerative diseases. The patient with neurodegenerative diseases often experiences profound disruptions in their circadian rhythms and/or sleep/wake cycles. In addition, a growing body of recent evidence implicates sleep disorders as an early symptom of neurodegenerative diseases, and also suggests that abnormalities in the circadian system lead to the onset and expression of neurodegenerative diseases. The genetic mutations which cause the pathogenesis of familial neurodegenerative diseases have been well studied; however, with the exception of Huntington’s disease, the majority of neurodegenerative diseases are sporadic. Interestingly, the dysfunction of microRNA is increasingly recognized as a cause of sporadic neurodegenerative diseases through the deregulated genes related to the pathogenesis of neurodegenerative disease, some of which are the causative genes of familial neurodegenerative diseases. Here we review the interplay of circadian rhythm disruption, sleep disorders and neurodegenerative disease, and its relation to microRNA, a key regulator of cellular processes. Full article
(This article belongs to the Special Issue Crosstalk between Circadian Rhythm and Diseases)
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