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Int. J. Mol. Sci. 2016, 17(8), 1208; doi:10.3390/ijms17081208

One-Carbon Metabolism in Prostate Cancer: The Role of Androgen Signaling

1
Department of Pathology, Oklahoma University Health Sciences Center, Oklahoma City, OK 73104, USA
2
Department of Pathology, Oklahoma University Health Sciences Center and Stephenson Cancer Center, Oklahoma City, OK 73104, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Li Yang
Received: 22 June 2016 / Revised: 16 July 2016 / Accepted: 18 July 2016 / Published: 27 July 2016
(This article belongs to the Special Issue Tumor Microenvironment and Metabolism)
View Full-Text   |   Download PDF [905 KB, uploaded 27 July 2016]   |  

Abstract

Cancer cell metabolism differs significantly from the metabolism of non-transformed cells. This altered metabolic reprogramming mediates changes in the uptake and use of nutrients that permit high rates of proliferation, growth, and survival. The androgen receptor (AR) plays an essential role in the establishment and progression of prostate cancer (PCa), and in the metabolic adaptation that takes place during this progression. In its role as a transcription factor, the AR directly affects the expression of several effectors and regulators of essential catabolic and biosynthetic pathways. Indirectly, as a modulator of the one-carbon metabolism, the AR can affect epigenetic processes, DNA metabolism, and redox balance, all of which are important factors in tumorigenesis. In this review, we focus on the role of AR-signaling on one-carbon metabolism in tumorigenesis. Clinical implications of one-carbon metabolism and AR-targeted therapies for PCa are discussed in this context. View Full-Text
Keywords: one-carbon metabolism; androgen receptor; epigenetics; methylation; polyamine metabolism; transsufluration one-carbon metabolism; androgen receptor; epigenetics; methylation; polyamine metabolism; transsufluration
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Corbin, J.M.; Ruiz-Echevarría, M.J. One-Carbon Metabolism in Prostate Cancer: The Role of Androgen Signaling. Int. J. Mol. Sci. 2016, 17, 1208.

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