Dietary Factors and Epigenetic Regulation for Prostate Cancer Prevention
Author(s) -
Emily Ho,
Laura M. Beaver,
David E. Williams,
Roderick H. Dashwood
Publication year - 2011
Publication title -
advances in nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.362
H-Index - 90
eISSN - 2156-5376
pISSN - 2161-8313
DOI - 10.3945/an.111.001032
Subject(s) - epigenetics , epigenome , dna methylation , biology , microrna , histone , cancer epigenetics , carcinogenesis , prostate cancer , cancer , genetics , cancer research , bioinformatics , gene expression , gene , histone methyltransferase
The role of epigenetic alterations in various human chronic diseases has gained increasing attention and has resulted in a paradigm shift in our understanding of disease susceptibility. In the field of cancer research, e.g., genetic abnormalities/mutations historically were viewed as primary underlying causes; however, epigenetic mechanisms that alter gene expression without affecting DNA sequence are now recognized as being of equal or greater importance for oncogenesis. Methylation of DNA, modification of histones, and interfering microRNA (miRNA) collectively represent a cadre of epigenetic elements dysregulated in cancer. Targeting the epigenome with compounds that modulate DNA methylation, histone marks, and miRNA profiles represents an evolving strategy for cancer chemoprevention, and these approaches are starting to show promise in human clinical trials. Essential micronutrients such as folate, vitamin B-12, selenium, and zinc as well as the dietary phytochemicals sulforaphane, tea polyphenols, curcumin, and allyl sulfur compounds are among a growing list of agents that affect epigenetic events as novel mechanisms of chemoprevention. To illustrate these concepts, the current review highlights the interactions among nutrients, epigenetics, and prostate cancer susceptibility. In particular, we focus on epigenetic dysregulation and the impact of specific nutrients and food components on DNA methylation and histone modifications that can alter gene expression and influence prostate cancer progression.
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