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

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...

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Autores principales: Blair, Lauren P., Cao, Jian, Zou, Mike Ran, Sayegh, Joyce, Yan, Qin
Formato: Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2011
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085456/
https://www.ncbi.nlm.nih.gov/pubmed/21544224
http://dx.doi.org/10.3390/cancers3011383
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author Blair, Lauren P.
Cao, Jian
Zou, Mike Ran
Sayegh, Joyce
Yan, Qin
author_facet Blair, Lauren P.
Cao, Jian
Zou, Mike Ran
Sayegh, Joyce
Yan, Qin
author_sort Blair, Lauren P.
collection PubMed
description 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.
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spelling pubmed-30854562011-05-02 Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer Blair, Lauren P. Cao, Jian Zou, Mike Ran Sayegh, Joyce Yan, Qin Cancers (Basel) Review 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. Molecular Diversity Preservation International (MDPI) 2011-03-16 /pmc/articles/PMC3085456/ /pubmed/21544224 http://dx.doi.org/10.3390/cancers3011383 Text en © 2011 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Blair, Lauren P.
Cao, Jian
Zou, Mike Ran
Sayegh, Joyce
Yan, Qin
Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer
title Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer
title_full Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer
title_fullStr Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer
title_full_unstemmed Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer
title_short Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer
title_sort epigenetic regulation by lysine demethylase 5 (kdm5) enzymes in cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085456/
https://www.ncbi.nlm.nih.gov/pubmed/21544224
http://dx.doi.org/10.3390/cancers3011383
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