Circadian gene variants in cancer

Kettner, Nicole M.; Katchy, Chinenye A.; Fu, Loning

doi:10.3109/07853890.2014.914808

Cited by 102 publications

(98 citation statements)

References 295 publications

(294 reference statements)

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“…Clock genes operate like oscillators, modulating rhythmic transcription of a large number of genes in all cells by a mechanism that relies on coordinated chromatin remodeling events (4,5). Situations that alter the normal expression pattern of the clock genes have important repercussions at the systemic, cellular and molecular levels (6).…”

Section: Introductionmentioning

confidence: 99%

Histone deacetylase inhibitors induce the expression of tumor suppressor genes Per1 and Per2 in human gastric cancer cells

et al. 2018

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Abstract. Period circadian regulator (Per)1 and Per2 genes are involved in the molecular mechanism of the circadian clock, and exhibit tumor suppressor properties. Several studies have reported a decreased expression of Per1, Per2 and Per3 genes in different types of cancer and cancer cell lines. Promoter methylation downregulates Per1, Per2 or Per3 expression in myeloid leukemia, breast, lung, and other cancer cells; whereas histone deacetylase inhibitors (HDACi) upregulate Per1 or Per3 expression in certain cancer cell lines. However, the transcriptional regulation of Per1 and Per2 in cancer cells by chromatin modifications is not fully understood. The present study aimed to determine whether HDACi regulate Per1 and Per2 expression in gastric cancer cell lines, and to investigate changes in chromatin modifications in response to HDACi. Treatment of KATO III and NCI-N87 human gastric cancer cells with sodium butyrate (NaB) or Trichostatin A (TSA) induced Per1 and Per2 mRNA expression in a dose-dependent manner. Chromatin immunoprecipitaion assays revealed that NaB and TSA decreased lysine 9 trimethylation on histone H3 (H3K9me3) at the Per1 promoter. TSA, but not NaB increased H3K9 acetylation at the Per2 promoter. It was also observed that binding of Sp1 and Sp3 to the Per1 promoter decreased following NaB treatment, whereas Sp1 binding increased at the Per2 promoter of NaB-and TSA-treated cells. In addition, Per1 promoter is not methylated in KATO III cells, while Per2 promoter was methylated, although NaB, TSA, and 5-Azacytidine do not change the methylated CpGs analyzed. In conclusion, HDACi induce Per1 and Per2 expression, in part, through mechanisms involving chromatin remodeling at the proximal promoter of these genes; however, other indirect mechanisms triggered by these HDACi cannot be ruled out. These findings reveal a previously unappreciated regulatory pathway between silencing of Per1 gene by H3K9me3 and upregulation of Per2 by HDACi in cancer cells.

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Section: Introductionmentioning

confidence: 99%

Histone deacetylase inhibitors induce the expression of tumor suppressor genes Per1 and Per2 in human gastric cancer cells

et al. 2018

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“…There is a large and growing literature on the effects of circadian gene knockouts (KO) in mice, and polymorphisms in humans, on disease risk [57][58][59][60][61][62][63]. These studies suggest the possibility that absent or altered function of circadian genes may increase the risk of some diseases in people.…”

Section: Molecular Epidemiology: Circadian Genes and Diseasementioning

confidence: 99%

Electric light, particularly at night, disrupts human circadian rhythmicity: is that a problem?

Stevens

Zhu

2015

Phil. Trans. R. Soc. B

131

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Over the past 3 billion years, an endogenous circadian rhythmicity has developed in almost all life forms in which daily oscillations in physiology occur. This allows for anticipation of sunrise and sunset. This physiological rhythmicity is kept at precisely 24 h by the daily cycle of sunlight and dark. However, since the introduction of electric lighting, there has been inadequate light during the day inside buildings for a robust resetting of the human endogenous circadian rhythmicity, and too much light at night for a true dark to be detected; this results in circadian disruption and alters sleep/wake cycle, core body temperature, hormone regulation and release, and patterns of gene expression throughout the body. The question is the extent to which circadian disruption compromises human health, and can account for a portion of the modern pandemics of breast and prostate cancers, obesity, diabetes and depression. As societies modernize (i.e. electrify) these conditions increase in prevalence. There are a number of promising leads on putative mechanisms, and epidemiological findings supporting an aetiologic role for electric lighting in disease causation. These include melatonin suppression, circadian gene expression, and connection of circadian rhythmicity to metabolism in part affected by haem iron intake and distribution.

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“…For example, in a study of Chinese men, individuals that harbored a SNP in Npas2 had a decreased risk of developing prostate cancer, whereas those with an SNP in Cry2 had nearly double the risk of those that did not [24]. Similarly, other circadian polymorphisms have 1 Relevance of Circadian Rhythm in Cancer been linked to increased postmenopausal breast cancer risk ( Cry2), reduced risk of developing non-Hodgkins lymphoma ( Npas2), increased occurrence and development of non-small cell lung cancer, and increased survival in colorectal and hepatocellular carcinoma ( Clock and Per3, respectively) [25][26][27][28][29][30].…”

Section: Cancer and The Clockmentioning

confidence: 99%

Relevance of Circadian Rhythm in Cancer

DiTacchio

Panda

2015

Energy Balance and Cancer

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Circadian rhythms are patterns of behavior, physiology, and metabolism that occur within a period of approximately 24 h. These rhythms are generated endogenously, but synchronize to external cues, thus enabling organisms to beneficially align physiological processes to the inherently dynamic, yet predictable, seasonal changes in the day-night cycle. The cell autonomous circadian oscillator temporally coordinates cellular processes, including metabolism, proliferation, cell signaling, organelle function, proteostasis, and DNA damage repair to sustain cellular homeostasis. It is hypothesized that the circadian oscillators evolved as a "flight from light" mechanism to minimize UV damage to single stranded DNA by restricting DNA replication to the nighttime. Support for this hypothesis is accumulating with the recent observation that the circadian rhythm and cell cycle are intimately coupled to each other, so that specific phases of cell cycle occur at a defined phase of the circadian oscillator at single-cell level [1]. Furthermore, chronic circadian disruption perturbs cellular homeostasis and predisposes to cancer. Conversely, numerous cancer cell lines display severe circadian alterations, which likely contribute to aggressive proliferation of the tumor. Hence, it is becoming increasingly important to understand the relevance of circadian rhythm for optimizing fitness

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Circadian gene variants in cancer

Cited by 102 publications

References 295 publications

Histone deacetylase inhibitors induce the expression of tumor suppressor genes Per1 and Per2 in human gastric cancer cells

Histone deacetylase inhibitors induce the expression of tumor suppressor genes Per1 and Per2 in human gastric cancer cells

Electric light, particularly at night, disrupts human circadian rhythmicity: is that a problem?

Relevance of Circadian Rhythm in Cancer

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