Targeting the epigenome with bioactive food components for cancer prevention

Thomas Prates Ong1, Fernando Salvador Moreno, Sharon Ann Ross

  • 1Laboratory of Diet, Nutrition and Cancer, Department of Food and Experimental Nutrition, Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil. tong@usp.br

Insights

Dietary bioactive food components (BFCs) can influence epigenetic processes like DNA methylation, potentially preventing cancer. More research is needed on effective doses and timing, especially regarding early-life nutrition, to clarify diet

Area of Science:

  • Epigenetics
  • Nutritional Science
  • Cancer Prevention

Background:

  • Epigenetic alterations, including DNA hypomethylation and histone modifications, are hallmarks of cancer, contributing to genomic instability and altered gene expression.
  • Epigenetic deregulation occurs early in carcinogenesis and is potentially reversible, making the epigenome a promising target for cancer prevention strategies.

Purpose of the Study:

  • To explore the role of bioactive food components (BFCs) in influencing epigenetic processes relevant to cancer prevention.
  • To highlight the need for further in vivo studies, particularly in humans, to understand the mechanisms of dietary influence on cancer prevention.

Main Methods:

  • Review of existing literature on BFCs (e.g., folate, polyphenols, selenium) and their impact on DNA methylation and histone modifications.
  • Discussion of the effects of these epigenetic modifications on genes involved in cell proliferation, death, and differentiation.

Main Results:

  • BFCs possess anticancer potential by influencing DNA methylation and histone modification processes.
  • Dietary components affect the expression of key cancer-related genes.

Conclusions:

  • The epigenome is a promising target for cancer prevention through BFCs, but in vivo human data and mechanistic understanding are limited.
  • Further research is crucial to determine effective doses and timing of BFCs for epigenetic effects, including the impact of early-life nutrition on cancer risk programming.

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