Mechanisms of Breast Cancer in Shift Workers: DNA Methylation in Five Core Circadian Genes in Nurses Working Night Shifts.
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Authors
Samulin Erdem, JohannaSkare, Øivind
Petersen-Øverleir, Marte
Notø, Heidi Ødegaard
Lie, Jenny-Anne S
Reszka, Edyta
Pepłońska, Beata
Zienolddiny, Shanbeh
Issue Date
2017
Metadata
Show full item recordAbstract
Shift work has been suggested to be associated with breast cancer risk, and circadian disruption in shift workers is hypothesized as one of the mechanisms of increased cancer risk. There is, however, insufficient molecular evidence supporting this hypothesis. Using the quantitative methodology of pyrosequencing, epigenetic changes in 5-methyl cytosine (5mC) in five circadian genes CLOCK, BMAL1, CRY1, PER1 and PER2 in female nurses working night shift work (278 breast cancer cases, 280 controls) were analyzed. In breast cancer cases, a medium exposure to night work was associated with increased methylation levels of the CLOCK (p=0.050), BMAL1 (p=0.001) and CRY1 (p=0.040) genes, compared with controls. Within the cases, analysis of the effects of shift work on the methylation patterns showed that methylation of CRY1 was lower in those who had worked night shift and had a high exposure (p=0.006) compared with cases that had worked only days. For cases with a medium exposure to night work, an increase in BMAL1 (p=0.003) and PER1 (p=0.035) methylation was observed compared with day working (unexposed) cases. The methylation levels of the five core circadian genes were also analyzed in relation to the estrogen and progesterone receptors status of the tumors in the cases, and no correlations were observed. Furthermore, nineteen polymorphisms in the five circadian genes were assessed for their effects on the methylation levels of the respective genes, but no associations were found. In summary, our data suggest that epigenetic regulation of CLOCK, BMAL1, CRY1 and PER1 may contribute to breast cancer in shift workers.Citation
J Cancer 2017, 8 (15):2876-2884Journal
Journal of CancerPubMed ID
28928877Additional Links
http://www.jcancer.org/v08p2876.htmType
ArticleLanguage
enISSN
1837-9664Sponsors
This project was supported by the Norway Grants, under the Polish-Norwegian Research Program (Grant no. Pol-Nor/196940/22/2013-clock shift). JSE acknowledges a postdoctoral fellowship from NIOH.ae974a485f413a2113503eed53cd6c53
10.7150/jca.21064
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Except where otherwise noted, this item's license is described as Archived with thanks to Journal of Cancer
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