Elsevier

The Journal of Nutrition

Volume 139, Issue 12, December 2009, Pages 2393-2396
The Journal of Nutrition

Dietary Sulforaphane, a Histone Deacetylase Inhibitor for Cancer Prevention

1 Presented as part of the symposium entitled “Nutrients and Epigenetic Regulation of Gene Expression” at the Experimental Biology 2009 meeting, April 20, 2009, in New Orleans, LA. This symposium was sponsored the American Society for Nutrition (ASN) and had no outside support declared. The Guest Editor for this symposium publication was Kevin Schalinske. Guest Editor disclosure: no relationships to disclose.
https://doi.org/10.3945/jn.109.113332Get rights and content
Under an Elsevier user license
open archive

Abstract

The reversible acetylation of histones is an important mechanism of gene regulation. During prostate cancer progression, specific modifications in acetylation patterns on histones are apparent. Targeting the epigenome, including the use of histone deacetylase (HDAC) inhibitors, is a novel strategy for cancer chemoprevention. Recently, drugs classified as HDAC inhibitors have shown promise in cancer clinical trials. We have previously found that sulforaphane (SFN), a compound found in cruciferous vegetables, inhibits HDAC activity in human colorectal and prostate cancer cells. Based on the similarity of SFN metabolites and other phytochemicals to known HDAC inhibitors, we previously demonstrated that sulforaphane acted as an HDAC inhibitor in the prostate, causing enhanced histone acetylation, derepression of P21 and Bax, and induction of cell cycle arrest/apoptosis, leading to cancer prevention. The ability of SFN to target aberrant acetylation patterns, in addition to effects on phase 2 enzymes, may make it an effective chemoprevention agent. These studies are important because of the potential to qualify or change recommendations for high-risk prostate cancer patients and thereby increase their survival through simple dietary choices incorporating easily accessible foods into their diets. These studies also will provide a strong scientific foundation for future large-scale human clinical intervention studies.

Abbreviations used:

GSH
glutathione
GST
glutathione-S-transferase
HAT
histone acetyltransferase
HDAC
histone deacetylase
ITC
isothiocyanate
NAC
N-acetylcysteine
Nrf2
nuclear-related factor 2
SAHA
suberoylanilide hydroxamic acid
SFN
sulforaphane

Cited by (0)

3

E. Ho, J. D. Clarke, and R. H. Dashwood, no conflicts of interest.