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Histone Demethylases in Prostate Cancer

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Nuclear Signaling Pathways and Targeting Transcription in Cancer

Abstract

Accumulating evidence has suggested that epigenetic alternations are as important as genetic mutations in cancer development. It is proposed that tumors are arisen by “malignant reprogramming” driven by a combination of both genetic and epigenetic changes. It therefore comes as no surprise that histone demethylases, the newest members of the histone modifying enzymes, are found to be targets of mutations and dysregulation in cancer cells. In this review article, we provide an overview of the types of histone demethylases whose genetic structure or expression is altered in cancers, the action of histone demethylases in cancer development and their potential inhibitors. Special emphasis is placed on the roles of histone demethylases in prostate cancer progression.

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Abbreviations

AR:

Androgen receptor

ARE:

Androgen responsive elements

CDK:

Cyclin-dependent kinase

CGH:

Comparative genomic hybridization

CRPC:

Castration-resistant prostate cancer

ER:

Estrogen receptor

FAD:

Flavin adenine dinucleotide

HIF:

Hypoxia-induced transcription factor

HP1:

Heterochromatin protein 1

KDM:

Histone lysine demethylase

MEF:

Mouse embryonic fibroblast

MAO:

Monoamine oxidase

NOG:

N-oxalylglycine

PRC:

Polycomb repressive complex

SAHF:

Senescence-associated heterochromatic foci

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Acknowledgement

This work is supported by NIH and DOD grants to H.J.K. H.J.K. acknowledges the generous support from Auburn Community Cancer Endowment Fund.

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Correspondence to Hsing-Jien Kung Ph.D. .

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Wang, LY. et al. (2014). Histone Demethylases in Prostate Cancer. In: Kumar, R. (eds) Nuclear Signaling Pathways and Targeting Transcription in Cancer. Cancer Drug Discovery and Development. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4614-8039-6_15

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