Dietary sulforaphane, a histone deacetylase inhibitor for cancer prevention

Emily Ho; John D Clarke; Roderick H Dashwood

doi:10.3945/jn.109.113332

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Dietary sulforaphane, a histone deacetylase inhibitor for cancer prevention

Journal article

Open access

Peer reviewed

Dietary sulforaphane, a histone deacetylase inhibitor for cancer prevention

Emily Ho, John D Clarke and Roderick H Dashwood

The Journal of nutrition, Vol.139(12), pp.2393-2396

12/2009

DOI: https://doi.org/10.3945/jn.109.113332

Handle:

https://hdl.handle.net/2376/106622

PMID: 19812222

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Abstract

Genomic Instability

Thiocyanates - metabolism

Humans

Histone Deacetylase Inhibitors - administration & dosage

Biological Availability

Male

Jejunum - metabolism

Anticarcinogenic Agents - administration & dosage

Transcription, Genetic

Acetylation

Thiocyanates - administration & dosage

Histones - antagonists & inhibitors

Isothiocyanates

Prostatic Neoplasms - drug therapy

Anticarcinogenic Agents - therapeutic use

Thiocyanates - therapeutic use

Gene Expression Regulation

Rats

Histone Deacetylases - metabolism

Enzyme Inhibitors - therapeutic use

Brassica

Animals

Diet

Histone Deacetylase Inhibitors - therapeutic use

Histones - metabolism

Dietary Supplements

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.

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Title: Dietary sulforaphane, a histone deacetylase inhibitor for cancer prevention
Creators: Emily Ho - Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis OR 97331, USA. emily.ho@oregonstate.edu
John D Clarke
Roderick H Dashwood
Publication Details: The Journal of nutrition, Vol.139(12), pp.2393-2396
Academic Unit: Pharmaceutical Sciences, Department of
Publisher: United States
Grant note: CA122906 / NCI NIH HHS CA090890 / NCI NIH HHS P30 ES00210 / NIEHS NIH HHS CA065525 / NCI NIH HHS CA122959 / NCI NIH HHS
Identifiers: 99900546939301842
Language: English
Resource Type: Journal article