Article Text
Abstract
Night shift work has been linked to increased breast cancer risk, although, the biological mechanisms underlying the increased risk of cancer among night shift workers have not been fully recognised yet. Recently, it has been suggested that night shift work may contribute to epigenetic changes in the circadian rhythm genes. Given the existing evidence suggesting the association between environmental factors and changes in methylation status of some of the suppressor genes we hypothesised that rotating night work may also affect epigenetic changes in these genes. Thus the aim of our study was to assess the potential association between current rotating night shift work and levels of 5-methylcytosine in the promoter regions of selected suppressor genes.
The cross-sectional study included as many as 710 nurses and midwives (348 working on rotating night shifts and 362 working only during the day) aged 40–60 years. During in person interviews, information about occupational history and potential confounders was collected. DNA was isolated from leucocytes and promoter methylation status of selected genes related to cell division (TP53, CDKN1A, CDKN2A, BRCA1, BRCA2) was determined using quantitative methylation-specific real-time PCR assay (qMSP) method. Univariate and multivariate regression models were used to assess the association between current work at night and methylation status, with adjustment for age and folate intake.
The analysis did not reveal any statistically significant associations between current rotating night work and level of 5-methylcytosine within promoter regions of the studied genes. The only result of borderline significance (0.1>p>0.05) was observed for CDKN1A gene, with inverse association between current rotating night work and higher methylation level in the promoter region of this gene (OR = 0.75, 95% CI: 0.54–1.1).
The results of our study do not provide evidence that rotating night shift work may modify methylation level of the promoter regions of the cell cycle genes.