Circadian disruption and breast cancer: An epigenetic link?

Kochan, David Z; Kovalchuk, Olga

doi:10.18632/oncotarget.4343

Cited by 30 publications

(18 citation statements)

References 144 publications

(211 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The PER/CRY complexes are subsequently phosphorylated by casein kinase 1 epsilon (CK1ε), leading to PER and CRY degradation. Another negative feedback is represented by the nuclear receptor subfamily 1 group D members 1, and 2 (REV‐ERBα and β), and the retinoic acid receptor‐related orphan receptor alpha (RORα) proteins, which translocate into the nucleus to repress and promote BMAL1 expression, respectively . Sirtuin 1 (SIRT1) is reported to be involved in multiple disease processes that include cancer, and also in circadian clock regulation .…”

Section: Introductionmentioning

confidence: 99%

“…Another negative feedback is represented by the nuclear receptor subfamily 1 group D members 1, and 2 (REV-ERBα and β), and the retinoic acid receptor-related orphan receptor alpha (RORα) proteins, which translocate into the nucleus to repress and promote BMAL1 expression, respectively. 8 Sirtuin 1 (SIRT1) is reported to be involved in multiple disease processes that include cancer, and also in circadian clock regulation. 9 SIRT1 and PER2 constitute a reciprocal negative regulation loop that plays important roles in modulating hepatic circadian rhythmicity.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Melatonin modulates dysregulated circadian clocks in mice with diethylnitrosamine‐induced hepatocellular carcinoma

Sánchez

González‐Fernández

Crespo

et al. 2018

Journal of Pineal Research

View full text Add to dashboard Cite

Disruption of circadian rhythms, which are regulated by the circadian clock machinery, plays an important role in different long-term diseases including hepatocellular carcinoma (HCC). Melatonin has been reported to alleviate promotion and progression of HCC, but the potential contribution of circadian clock modulation is unknown. We investigated the effects of melatonin in mice which received diethylnitrosamine (DEN) (35 mg/kg body weight ip) once a week for 8 weeks. Melatonin was given at 5 or 10 mg kg d ip beginning 4 weeks after the onset of DEN administration and ending at the sacrifice time (10, 20, 30, or 40 weeks). Liver expression of Bmal1, Clock, Npas2, Rorα, and Sirt1 increased, whereas Cry1, Per1, Per2, Per3, CK1ε, Rev-erbα, and Rev-erbβ decreased following DEN administration. Melatonin treatment prevented changes in the expression of clock genes, and this effect was accompanied by an upregulation of the MT1 receptor and reduced levels of the hypoxia-inducible factors Hif-1α and Hif-2α. An increased expression of p21, p53, and PARP1/2, a higher Bax/Bcl-2 ratio, and a lower expression of Cyclin D1, CDK6, HSP70, HSP90, and GRP78 proteins were also observed in melatonin-treated mice. Melatonin significantly potentiated the suppression of proliferation and cell cycle arrest induced by the synthetic REV-ERB agonist SR9009 in human Hep3B cells, and BMAL1 knocking down attenuated the pro-apoptotic and antiproliferative effect of melatonin. Results support a contribution of changes in the circadian clock components to the beneficial effects of melatonin in HCC and highlight the usefulness of strategies modulating the circadian machinery in hepatocarcinogenesis.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Melatonin modulates dysregulated circadian clocks in mice with diethylnitrosamine‐induced hepatocellular carcinoma

Sánchez

González‐Fernández

Crespo

et al. 2018

Journal of Pineal Research

View full text Add to dashboard Cite

show abstract

“…Breast cancer (BC) is the most common malignancy affecting women, with 1.8 million newly diagnosed cases in 2013, and is the leading contributor to disability-adjusted life-years [2–4]. The incidence of BC is increasing worldwide, as is the effect of hereditary BC.…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in TIM-3 and breast cancer susceptibility in Chinese women: A case-control study

et al. 2016

View full text Add to dashboard Cite

Previous studies have found associations between polymorphisms in T cell immunoglobulin and mucin domain 3 (TIM-3) and increased risks of various cancers. However, the association between TIM-3 polymorphisms and breast cancer (BC) remains uncertain. In this study, a total of 560 BC patients and 583 age, sex, and ethnicity-matched healthy controls from Northwest China were included. The polymorphisms were genotyped using Sequenom MassARRAY. The expression level of TIM-3 protein was detected by immunohistochemistry. We observed rs10053538 had a significantly increased risk of BC, comparing with the wild-type genotype even after Bonferroni correction. In addition, the rs4704853 G>A variants were more frequent among BC patients than the controls (GA + AA vs. GG: OR = 1.32, 95% CI = 1.03-1.69, P = 0.026); However, the significance was lost after Bonferroni correction (P = 0.078). Furthermore, rs10053538 was associated with lymph node metastasis. Age stratification revealed that among patients aged <49 years, those with the rs4704853 GA/AA genotype had a higher risk of BC; But there was no difference when Bonferroni correction was conducted. Immunohistochemical analysis showed that the expression of TIM-3 protein in the breast cancer tissues was higher in patients carrying the rs10053538 GT+TT genotype than those with GG genotype (P = 0.012). However, we failed to find any difference between BC patients and controls in any rs1036199 genetic model. These findings suggested that rs10053538 in TIM-3 might increase susceptibility to BC and promote the progression of BC in Chinese women.

show abstract

“…Finally, epigenetic modification is a promising molecular mechanism for metabolic and oncostatic action of MLT, in response to environmental exposure to polluting sources, such as ALAN. These reversible modifications are profoundly associated with the expression of several genes related with obesity development [112] and carcinogenic activity [210].…”

Section: Mlt and Cancermentioning

confidence: 99%

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

Zubidat

Haim

2017

Journal of Basic and Clinical Physiology and Pharmacology

View full text Add to dashboard Cite

Both obesity and breast cancer are already recognized worldwide as the most common syndromes in our modern society. Currently, there is accumulating evidence from epidemiological and experimental studies suggesting that these syndromes are closely associated with circadian disruption. It has been suggested that melatonin (MLT) and the circadian clock genes both play an important role in the development of these syndromes. However, we still poorly understand the molecular mechanism underlying the association between circadian disruption and the modern health syndromes. One promising candidate is epigenetic modifications of various genes, including clock genes, circadian-related genes, oncogenes, and metabolic genes. DNA methylation is the most prominent epigenetic signaling tool for gene expression regulation induced by environmental exposures, such as artificial light-at-night (ALAN). In this review, we first provide an overview on the molecular feedback loops that generate the circadian regulation and how circadian disruption by ALAN can impose adverse impacts on public health, particularly metabolic disorders and breast cancer development. We then focus on the relation between ALAN-induced circadian disruption and both global DNA methylation and specific loci methylation in relation to obesity and breast cancer morbidities. DNA hypo-methylation and DNA hyper-methylation, are suggested as the most studied epigenetic tools for the activation and silencing of genes that regulate metabolic and monostatic responses. Finally, we discuss the potential clinical and therapeutic roles of MLT suppression and DNA methylation patterns as novel biomarkers for the early detection of metabolic disorders and breast cancer development.

show abstract

Circadian disruption and breast cancer: An epigenetic link?

Cited by 30 publications

References 144 publications

Melatonin modulates dysregulated circadian clocks in mice with diethylnitrosamine‐induced hepatocellular carcinoma

Melatonin modulates dysregulated circadian clocks in mice with diethylnitrosamine‐induced hepatocellular carcinoma

Polymorphisms in TIM-3 and breast cancer susceptibility in Chinese women: A case-control study

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

Contact Info

Product

Resources

About