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Prostate Cancer
Volume 2016, Article ID 8108549, 9 pages
http://dx.doi.org/10.1155/2016/8108549
Review Article

Hydrogen Sulfide Signaling Axis as a Target for Prostate Cancer Therapeutics

1Cardiovascular and Metabolic Research Unit, Lakehead University, Thunder Bay, ON, P7B 5E1, Canada
2Department of Health Sciences, Lakehead University, Thunder Bay, ON, P7B 5E1, Canada
3Department of Chemistry and Biochemistry, Laurentian University, Sudbury, ON, P3E 2C6, Canada

Received 19 October 2015; Accepted 28 January 2016

Academic Editor: David Nanus

Copyright © 2016 Mingzhe Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Hydrogen sulfide (H2S) was originally considered toxic at elevated levels; however just in the past decade H2S has been proposed to be an important gasotransmitter with various physiological and pathophysiological roles in the body. H2S can be generated endogenously from L-cysteine by multiple enzymes, including cystathionine gamma-lyase, cystathionine beta-synthase, and 3-mercaptopyruvate sulfurtransferase in combination with cysteine aminotransferase. Prostate cancer is a major health concern and no effective treatment for prostate cancers is available. H2S has been shown to inhibit cell survival of androgen-independent, androgen-dependent, and antiandrogen-resistant prostate cancer cells through different mechanisms. Various H2S-releasing compounds, including sulfide salts, diallyl disulfide, diallyl trisulfide, sulforaphane, and other polysulfides, also have been shown to inhibit prostate cancer growth and metastasis. The expression of H2S-producing enzyme was reduced in both human prostate cancer tissues and prostate cancer cells. Androgen receptor (AR) signaling is indispensable for the development of castration resistant prostate cancer, and H2S was shown to inhibit AR transactivation and contributes to antiandrogen-resistant status. In this review, we summarized the current knowledge of H2S signaling in prostate cancer and described the molecular alterations, which may bring this gasotransmitter into the clinic in the near future for developing novel pharmacological and therapeutic interventions for prostate cancer.