Selenium (Se) is an essential trace element. Methylselenocysteine (MSC) is an organic form of selenium obtained primarily through dietary ingestion. Selenium, especially MSC, showed significant inhibitory effect on mammary tumorigenesis, especially at early stages, in carcinogen-induced rat mammary tumor models. However the underlying mechanisms are not fully understood. Accumulating evidence indicates that disruption of circadian rhythm by shift work or jet lag increases the risk of breast, prostate, and colon cancers. About 10% of genes, including many genes involved in hormone signaling and DNA damage response and repair (DDRR), are under circadian control and as a result show significant oscillation in expression across the day. Recent mechanism studies demonstrated that MSC restored and enhanced circadian expression of major clock genes, especially Period 2 (Per2), and circadian-controlled genes to inhibit mammary tumorigenesis induced by carcinogens in rats. Moreover, MSC restores and enhances circadian gene expression by increasing NAD+/NADH and SIRT1 activity and modulated acetylation of circadian regulatory protein, BMAL1, and histone 3 associated with Per2 gene promoter. This chapter will focus on how the dietary chemopreventive regimen of MSC epigenetically modulates the circadian rhythm at molecular level and how it contributes to its chemopreventive activity.
CITATION STYLE
Zarbl, H., & Fang, M. (2019). Dietary methylselenocysteine and epigenetic regulation of circadian gene expression. In Handbook of Nutrition, Diet, and Epigenetics (Vol. 3, pp. 1915–1932). Springer International Publishing. https://doi.org/10.1007/978-3-319-55530-0_63
Mendeley helps you to discover research relevant for your work.