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Cancers 2011, 3(1), 1383-1404; doi:10.3390/cancers3011383

Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer

Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
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Received: 30 January 2011 / Revised: 7 March 2011 / Accepted: 8 March 2011 / Published: 16 March 2011
(This article belongs to the Special Issue Epigenetics of Cancer Progression)
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Abstract

Similar to genetic alterations, epigenetic aberrations contribute significantly to tumor initiation and progression. In many cases, these changes are caused by activation or inactivation of the regulators that maintain epigenetic states. Here we review our current knowledge on the KDM5/JARID1 family of histone demethylases. This family of enzymes contains a JmjC domain and is capable of removing tri- and di- methyl marks from lysine 4 on histone H3. Among these proteins, RBP2 mediates drug resistance while JARID1B is required for melanoma maintenance. Preclinical studies suggest inhibition of these enzymes can suppress tumorigenesis and provide strong rationale for development of their inhibitors for use in cancer therapy.
Keywords: KDM5; JARID1; RBP2; PLU1; SMCX; SMCY; LID; histone demethylase; cancer stem cell; drug resistance KDM5; JARID1; RBP2; PLU1; SMCX; SMCY; LID; histone demethylase; cancer stem cell; drug resistance
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This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Blair, L.P.; Cao, J.; Zou, M.R.; Sayegh, J.; Yan, Q. Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer. Cancers 2011, 3, 1383-1404.

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