Cancer Epigenetics: Mechanisms and Crosstalk of a HDAC Inhibitor, VorinostatJean Lee and Stephanie Huang R*
Department of Medicine, University of Chicago, USA
- *Corresponding Author:
- Stephanie Huang R
Department of Medicine
The University of Chicago, Chicago, IL 60637, USA
Tel: (773) 702-9363
Fax: (773) 702-0963
E-mail: [email protected]
Received date: May 13, 2013; Accepted date: May 30, 2013; Published date: June 05, 2013
Citation: Lee J, Huang RS (2013) Cancer Epigenetics: Mechanisms and Crosstalk of a HDAC Inhibitor, Vorinostat. Chemotherapy 2:111. doi: 10.4172/2167-7700.1000111
Copyright: © 2013 Lee J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In recent years, histone deacetylase inhibitors (HDACis), a novel class of agents that targets mechanistic abnormalities in cancers, have shown promising anti-cancer activity in both hematological and solid cancers. Among them, vorinostat was approved by FDA to treat cutaneous T-cell lymphoma and is being evaluated in other cancer types. Although initially designed to target histone deacetylase, vorinostat were found to have additional effects on other epigenetic machineries, for example acetylation of non-HDAC, methylation and microRNA (miRNA) expression. In this review, we examined all known mechanisms of action for vorinostat. We also summarized the current findings on the ‘crosstalk’ between different epigenetic machineries. These findings suggest that improved understanding of epigenetic regulatory role of vorinostat and/or other HDACis will provide novel insights in improving utilization of this class of novel agents.