Epigenetic diet: impact on the epigenome and cancer

Abstract

A number of bioactive dietary components are of particular interest in the field of epigenetics. Many of these compounds display anticancer properties and may play a role in cancer prevention. Numerous studies suggest that a number of nutritional compounds have epigenetic targets in cancer cells. Importantly, emerging evidence strongly suggests that consumption of dietary agents can alter normal epigenetic states as well as reverse abnormal gene activation or silencing. Epigenetic modifications induced by bioactive dietary compounds are thought to be beneficial. Substantial evidence is mounting proclaiming that commonly consumed bioactive dietary factors act to modify the epigenome and may be incorporated into an ‘epigenetic diet‘. Bioactive nutritional components of an epigenetic diet may be incorporated into one‘s regular dietary regimen and used therapeutically for medicinal or chemopreventive purposes. This article will primarily focus on dietary factors that have been demonstrated to influence the epigenome and that may be used in conjunction with other cancer prevention and chemotherapeutic therapies.

KEYWORDS::

• acetylation
• cancer
• dietary
• epigenetic
• methylation
• nutrigenomics

Acknowledgements

The authors thank Drs Yuanyuan Li and Syed M Meeran for helpful comments on this manuscript.

Financial & competing interests disclosure

This work was supported in part by grants from the National Cancer Institute (RO1 CA129415), the American Institute for Cancer Research, and the Norma Livingston Foundation. Tabitha M Hardy was supported by NIH National Institute of General Medical Sciences (NIGMS) Institutional Research and Academic Career Development Awards (IRACDA) Program 5K12GM088010 (Dr Bryan Noe [principal investigator]). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported in part by grants from the National Cancer Institute (RO1 CA129415), the American Institute for Cancer Research, and the Norma Livingston Foundation. Tabitha M Hardy was supported by NIH National Institute of General Medical Sciences (NIGMS) Institutional Research and Academic Career Development Awards (IRACDA) Program 5K12GM088010 (Dr Bryan Noe [principal investigator]). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.