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Histone deacetylases as targets for dietary cancer preventive agents: lessons learned with butyrate, diallyl disulfide, and sulforaphane.
Curr Drug Targets 2006; 7(4):443-52CD

Abstract

Cancer is a multi-factorial process involving genetic and epigenetic events which result in neoplastic transformation. Reversal of aberrant epigenetic events, including those that modulate the transcriptional activity of genes associated with various signaling pathways, holds the prospect of influencing multiple stages of tumorigenesis. Perturbation of normal histone acetylation status can result in undesirable phenotypic changes, including developmental disorders and cancer. Indeed, aberrant histone acetylation may be an etiological factor in several, if not all, types of cancer. In general, histone acetylation leads to chromatin remodeling and a de-repression of transcription. Histone deacetylase (HDAC) inhibitors may be useful for cancer prevention and therapy by virtue of their ability to 'reactivate' the expression of epigenetically silenced genes, including those involved in differentiation, cell cycle regulation, apoptosis, angiogenesis, invasion, and metastasis. Several natural and synthetic HDAC inhibitors have been shown to affect the growth and survival of tumor cells in vitro and in vivo. Interestingly, three dietary chemopreventive agents, butyrate, diallyl disulfide, and sulforaphane, also have HDAC inhibitory activity. This review discusses the role of aberrant histone acetylation in tumorigenesis and describes the potential for cancer chemoprevention and therapy with a particular emphasis on dietary HDAC inhibitors.

Authors+Show Affiliations

Linus Pauling Institute, Weniger 503, Oregon State University, Corvallis, 97331-6512, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

16611031

Citation

Myzak, Melinda C., and Roderick H. Dashwood. "Histone Deacetylases as Targets for Dietary Cancer Preventive Agents: Lessons Learned With Butyrate, Diallyl Disulfide, and Sulforaphane." Current Drug Targets, vol. 7, no. 4, 2006, pp. 443-52.
Myzak MC, Dashwood RH. Histone deacetylases as targets for dietary cancer preventive agents: lessons learned with butyrate, diallyl disulfide, and sulforaphane. Curr Drug Targets. 2006;7(4):443-52.
Myzak, M. C., & Dashwood, R. H. (2006). Histone deacetylases as targets for dietary cancer preventive agents: lessons learned with butyrate, diallyl disulfide, and sulforaphane. Current Drug Targets, 7(4), pp. 443-52.
Myzak MC, Dashwood RH. Histone Deacetylases as Targets for Dietary Cancer Preventive Agents: Lessons Learned With Butyrate, Diallyl Disulfide, and Sulforaphane. Curr Drug Targets. 2006;7(4):443-52. PubMed PMID: 16611031.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Histone deacetylases as targets for dietary cancer preventive agents: lessons learned with butyrate, diallyl disulfide, and sulforaphane. AU - Myzak,Melinda C, AU - Dashwood,Roderick H, PY - 2006/4/14/pubmed PY - 2006/5/2/medline PY - 2006/4/14/entrez SP - 443 EP - 52 JF - Current drug targets JO - Curr Drug Targets VL - 7 IS - 4 N2 - Cancer is a multi-factorial process involving genetic and epigenetic events which result in neoplastic transformation. Reversal of aberrant epigenetic events, including those that modulate the transcriptional activity of genes associated with various signaling pathways, holds the prospect of influencing multiple stages of tumorigenesis. Perturbation of normal histone acetylation status can result in undesirable phenotypic changes, including developmental disorders and cancer. Indeed, aberrant histone acetylation may be an etiological factor in several, if not all, types of cancer. In general, histone acetylation leads to chromatin remodeling and a de-repression of transcription. Histone deacetylase (HDAC) inhibitors may be useful for cancer prevention and therapy by virtue of their ability to 'reactivate' the expression of epigenetically silenced genes, including those involved in differentiation, cell cycle regulation, apoptosis, angiogenesis, invasion, and metastasis. Several natural and synthetic HDAC inhibitors have been shown to affect the growth and survival of tumor cells in vitro and in vivo. Interestingly, three dietary chemopreventive agents, butyrate, diallyl disulfide, and sulforaphane, also have HDAC inhibitory activity. This review discusses the role of aberrant histone acetylation in tumorigenesis and describes the potential for cancer chemoprevention and therapy with a particular emphasis on dietary HDAC inhibitors. SN - 1389-4501 UR - https://www.unboundmedicine.com/medline/citation/16611031/Histone_deacetylases_as_targets_for_dietary_cancer_preventive_agents:_lessons_learned_with_butyrate_diallyl_disulfide_and_sulforaphane_ L2 - http://www.eurekaselect.com/55652/article DB - PRIME DP - Unbound Medicine ER -