title: Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition.
abstract: CONCLUSIONS
  Sulforaphane, produced by the hydrolytic conversion of glucoraphanin after ingestion of cruciferous vegetables, particularly broccoli and broccoli sprouts, has been extensively studied due to its apparent health-promoting properties in disease and limited toxicity in normal tissue. Recent Studies: Recent identification of a sub-population of tumor cells with stem cell-like self-renewal capacity that may be responsible for relapse, metastasis, and resistance, as a potential target of the dietary compound, may be an important aspect of sulforaphane chemoprevention. Evidence also suggests that sulforaphane may target the epigenetic alterations observed in specific cancers, reversing aberrant changes in gene transcription through mechanisms of histone deacetylase inhibition, global demethylation, and microRNA modulation.
  
  
  RESULTS
  In this review, we discuss the biochemical and biological properties of sulforaphane with a particular emphasis on the anticancer properties of the dietary compound. Sulforaphane possesses the capacity to intervene in multistage carcinogenesis through the modulation and/or regulation of important cellular mechanisms. The inhibition of phase I enzymes that are responsible for the activation of pro-carcinogens, and the induction of phase II enzymes that are critical in mutagen elimination are well-characterized chemopreventive properties. Furthermore, sulforaphane mediates a number of anticancer pathways, including the activation of apoptosis, induction of cell cycle arrest, and inhibition of NFκB.
  
  
  CONCLUSIONS
  Further characterization of the chemopreventive properties of sulforaphane and its capacity to be selectively toxic to malignant cells are warranted to potentially establish the clinical utility of the dietary compound as an anti-cancer compound alone, and in combination with clinically relevant therapeutic and management strategies.
authors.affiliation: 1 Epigenomic Medicine, Baker IDI Heart and Diabetes Institute, The Alfred Medical Research and Education Precinct , Melbourne, Australia .
authors.forename: Stephanie M
authors.initials: SM
authors.lastname: Tortorella
authors.forename: Simon G
authors.initials: SG
authors.lastname: Royce
authors.forename: Paul V
authors.initials: PV
authors.lastname: Licciardi
authors.forename: Tom C
authors.initials: TC
authors.lastname: Karagiannis
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D018890:Chemoprevention; D019587:Dietary Supplements; D063185:Epigenetic Repression / Q000235:genetics*; D056572:Histone Deacetylase Inhibitors / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D006655:Histone Deacetylases / Q000378:metabolism*; D006801:Humans; D017879:Isothiocyanates / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D009369:Neoplasms / Q000178:diet therapy* / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D013454:Sulfoxides
chemical_list: D016588:Anticarcinogenic Agents; D056572:Histone Deacetylase Inhibitors; D017879:Isothiocyanates; D013454:Sulfoxides; D006655:Histone Deacetylases; C016766:sulforaphane