Dietary agents as histone deacetylase inhibitors

Melinda C Myzak1, Emily Ho, Roderick H Dashwood

  • 1Linus Pauling Institute, Oregon State University, Corvallis, Oregon 97331-6512, USA.

Insights

Dietary agents like butyrate, DADS, and SFN show histone deacetylase (HDAC) inhibitory activity. These weak ligands may offer cancer prevention by subtly regulating genes involved in cell growth and apoptosis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Cancer cells exhibit an imbalance in histone acetyltransferase (HAT) and histone deacetylase (HDAC) activity.
  • HDAC inhibitors disrupt cancer cell cycles and induce apoptosis by derepressing genes like P21 and BAX.
  • Potent HDAC inhibitors are sought for cancer therapy, but weaker ligands for cancer prevention are often overlooked.

Purpose of the Study:

  • To explore the potential of dietary agents as HDAC inhibitors for cancer prevention.
  • To differentiate between pharmacologic HDAC inhibitors and dietary HDAC inhibitors.
  • To investigate the role of dietary HDAC inhibitors in modulating gene expression for cellular defense.

Main Methods:

  • Review of existing literature on HDAC inhibitors and dietary agents.
  • In vitro and in vivo studies of HDAC inhibitory activity of agents like butyrate, DADS, and SFN.
  • Analysis of gene expression changes related to cell cycle and apoptosis.

Main Results:

  • Butyrate, DADS, and SFN demonstrate HDAC inhibitory activity.
  • Dietary HDAC inhibitors act as weak ligands, subtly regulating gene expression.
  • Pharmacologic HDAC inhibitors potently derepress gene expression for therapeutic intervention.

Conclusions:

  • Dietary agents can possess HDAC inhibitory properties, suggesting a role in cancer prevention.
  • Weak HDAC inhibition by dietary compounds may offer a distinct approach to cancer chemoprevention.
  • Further research is needed to understand how dietary HDAC inhibitors enhance normal cell responses to external stimuli.

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