Upregulation of circadian gene 'hClock' contribution to metastasis of colorectal cancer

Wang, Yaping; Sun, Ninghui; Lü, Chao; Bei, Yi‐Bing; Ran, Qian; Hua, Lingyang

doi:10.3892/ijo.2017.3987

Cited by 32 publications

(27 citation statements)

References 38 publications

(38 reference statements)

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“…Importantly, mice with mutations in the Bmal1 gene show premature aging phenotype [15]. In addition, human CLOCK has been suggested to be involved in metastasis of colorectal cancer [16]. These findings implicate the core circadian machinery in the regulation of DDR and the cell cycle.…”

Section: Possible Roles Of Clock Proteins In Functional Regulation Ofmentioning

confidence: 97%

A Molecular Link between the Circadian Clock, DNA Damage Responses, and Oncogene Activation

Okamoto‐Uchida¹,

Izawa²,

Hirayama³

2019

Oncogenes and Carcinogenesis

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Circadian clocks enhance the efficiency and survival of living things by organizing their behavior and body functions. There has been a long history of research seeking a link between circadian clock and tumorigenesis. Studies of animal models and human tumor samples have revealed that the dysregulation of circadian clocks is an important endogenous factor causing mammalian cancer development. The core circadian clock regulators have been implicated in the control of both the cell cycle and DNA damage responses (DDR). Conversely, several intracellular signaling cascades that play important roles in regulation of the cell cycle and the DDR also contribute to circadian clock regulation. This review describes selected regulatory aspects of circadian clocks, providing evidence of a molecular link of the circadian clocks with cellular DDR.

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Section: Possible Roles Of Clock Proteins In Functional Regulation Ofmentioning

confidence: 97%

A Molecular Link between the Circadian Clock, DNA Damage Responses, and Oncogene Activation

Okamoto‐Uchida¹,

Izawa²,

Hirayama³

2019

Oncogenes and Carcinogenesis

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“…CLOCK k/d cells also had reduced metastatic potential in mice and reduced expression of HIF1α, ARNT and VEGF, all known to be key players in angiogenesis (Wang et al, 2017). In vitro, SW620 cells endogenously expressing high levels of CLOCK showed decreased proliferation and decreased cell migration after CLOCK k/d, while CLOCK overexpression in an endogenously low expressing cell line, SW480, resulted in the opposite effect (Wang et al, 2015b, Wang et al, 2017. CLOCK k/d in U87MG cells (human glioblastoma) increased apoptosis, along with decreased MYC and CCNB1 (Cyclin B1) (Wang et al, 2016).…”

Section: Clockmentioning

confidence: 99%

“…Mechanistic interrogation found that overexpressing CLOCK caused a decrease in apoptosis related proteins BAX and BID and an increase in p-AKT (Wang et al, 2015b). CLOCK k/d cells also had reduced metastatic potential in mice and reduced expression of HIF1α, ARNT and VEGF, all known to be key players in angiogenesis (Wang et al, 2017). In vitro, SW620 cells endogenously expressing high levels of CLOCK showed decreased proliferation and decreased cell migration after CLOCK k/d, while CLOCK overexpression in an endogenously low expressing cell line, SW480, resulted in the opposite effect (Wang et al, 2015b, Wang et al, 2017.…”

Section: Clockmentioning

confidence: 99%

Cancer clocks in tumourigenesis: the p53 pathway and beyond

Stephenson

Usselmann

Tergaonkar

et al. 2021

Endocrine-Related Cancer

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Circadian rhythms regulate a vast array of physiological and cellular processes, as well as the hormonal milieu, to keep our cells synchronised to the light-dark cycle. Epidemiologic studies have implicated circadian disruption in the development of breast and other cancers, and numerous clock genes are dysregulated in human tumours. Here we review the evidence that circadian rhythms, when altered at the molecular level, influence cancer growth. We also note some common pitfalls in circadian-cancer research and how they might be avoided to maximise comparable results and minimise misleading data. Studies of circadian gene mutant mice, and human cancer models in vitro and in vivo, demonstrate that clock genes can impact tumourigenesis. Clock genes influence important cancer related pathways, ranging from p53-mediated apoptosis to cell cycle progression. Confusingly, clock dysfunction can be both pro- or anti- tumourigenic in a model and cell type specific manner. Due to this duality, there is no canonical mechanism for clock interaction with tumourigenic pathways. To understand the role of the circadian clock in patients’ tumours requires analysis of the molecular clock status compared to healthy tissue. Novel mathematical approaches are under development, but this remains largely aspirational, and is hampered by a lack of temporal information in publicly available datasets. Current evidence broadly supports the notion that the circadian clock is important for cancer biology. More work is necessary to develop an overarching model of this connection. Future studies would do well to analyse the clock network in addition to alterations in single clock genes.

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“…Female nurses with long-term rotating night shift work had an increased risk for breast cancer (30). In addition, increased expression of the circadian gene hClock may contribute to tumorigenesis, such as the metastasis of colorectal cancer, through the enhanced expression of angiogenesis-related genes (31). …”

Section: Circadian Rhythm In Degenerative Disease and Cancermentioning

confidence: 99%

Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer

Maiese¹

2017

CNR

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Background The mammalian circadian clock and its associated clock genes are increasingly be recognized as critical components for a number of physiological and disease processes that extend beyond hormone release, thermal regulation, and sleep-wake cycles. New evidence suggests that clinical behavior disruptions that involve prolonged shift work and even space travel may negatively impact circadian rhythm and lead to multi-system disease. Methods In light of the significant role circadian rhythm can hold over the body's normal physiology as well as disease processes, we examined and discussed the impact circadian rhythm and clock genes hold over lifespan, neurodegenerative disorders, and tumorigenesis. Results In experimental models, lifespan is significantly reduced with the introduction of arrhythmic mutants and leads to an increase in oxidative stress exposure. Interestingly, patients with Alzheimer's disease and Parkinson's disease may suffer disease onset or progression as a result of alterations in the DNA methylation of clock genes as well as prolonged pharmacological treatment for these disorders that may lead to impairment of circadian rhythm function. Tumorigenesis also can occur with the loss of a maintained circadian rhythm and lead to an increased risk for nasopharyngeal carcinoma, breast cancer, and metastatic colorectal cancer. Interestingly, the circadian clock system relies upon the regulation of the critical pathways of autophagy, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), and silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) as well as proliferative mechanisms that involve the wingless pathway of Wnt/β-catenin pathway to foster cell survival during injury and block tumor cell growth. Conclusions Future targeting of the pathways of autophagy, mTOR, SIRT1, and Wnt that control mammalian circadian rhythm may hold the key for the development of novel and effective therapies against aging- related disorders, neurodegenerative disease, and tumorigenesis.

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Upregulation of circadian gene 'hClock' contribution to metastasis of colorectal cancer

Cited by 32 publications

References 38 publications

A Molecular Link between the Circadian Clock, DNA Damage Responses, and Oncogene Activation

A Molecular Link between the Circadian Clock, DNA Damage Responses, and Oncogene Activation

Cancer clocks in tumourigenesis: the p53 pathway and beyond

Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer

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