Targeting the Epigenome with Bioactive Food Components for Cancer Prevention

Abstract

Epigenetic processes participate in cancer development and likely influence cancer prevention. Global DNA hypomethylation, gene promoter hypermethylation and aberrant histone posttranslational modifications are hallmarks of neoplastic cells which have been associated with genomic instability and altered gene expression. Because epigenetic deregulation occurs early in carcinogenesis and is potentially reversible, intervention strategies targeting the epigenome have been proposed for cancer prevention. Bioactive food components (BFCs) with anticancer potential, including folate, polyphenols, selenium, retinoids, fatty acids, isothiocyanates and allyl compounds, influence DNA methylation and histone modification processes. Such activities have been shown to affect the expression of genes involved in cell proliferation, death and differentiation that are frequently altered in cancer. Although the epigenome represents a promising target for cancer prevention with BFCs, few studies have addressed the influence of dietary components on these mechanisms in vivo, particularly on the phenotype of humans, and thus the exact mechanisms whereby diet mediates an effect on cancer prevention remains unclear. Primary factors that should be elucidated include the effective doses and dose timing of BFCs to attain epigenetic effects. Because diet-epigenome interactions are likely to occur in utero, the impact of early-life nutrition on cancer risk programming should be further investigated.

Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21waf-1

“…Hydroxyurea, resveratrol, and pyrithione induce premature senescence by ROS generation (Luo et al 2013;Ong et al 2011). Thus, drug targeting premature senescence in cancer cells could be a superior approach rather activating apoptosis because at a lower concentration of the drug, activated senescence regresses the tumor growth by neutralizing the toxicity of the drugs (Wu et al 2007).…”

Brazilian Society for Food and Nutrition position statement: nutrigenetic tests

“…Some nutrients that modulate epigenetic events include (but are not limited to) amino acids such as lysine (required for modifications on histone residues); methionine (precursor of S-adenosylmethionine (SAM-methyl donor); short chain fatty acids such as butyric acid; vitamins or similar essential compounds, especially vitamins B 2 , B 6 , B 12 , and folic acid, choline and betaine; and minerals such as magnesium and zinc [49,50]. Specific nutrients are needed to boost metabolic pathways that result in methylation and both scarcity and excess of these nutrients can directly affect the epigenome.…”

Genomics in Primary and Secondary Prevention of Pancreatic Cancer

“…It has been proposed that epigenetic variation depends on external factors such as tobacco and arsenic among others, and that it may play an important role in aging and diseases such as cancer, type 2 diabetes, and metabolic disorders. There is some evidence supporting that methylation levels are potentially modifiable through diet, providing a unique opportunity for primary prevention interventions [23] . The methylomes of multiple types of tumours are currently being deciphered in the context of several worldwide consortia [24] .…”