Unsuspected protumorigenic signaling role for the oncometabolite GABA in advanced prostate cancer

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Abstract

Elucidating the events that underpin the transition from androgen-dependent to castrate-resistant prostate cancer (CRPC) remains a clinical challenge. In this issue of Cancer Research, Gao and colleagues identify that the g-aminobutyric acid (GABA) shunt is upregulated with the onset of CRPC, via phosphorylation and activation of glutamate decarboxylase (GAD) 65. Overproduction of GABA, an oncometabolite, can directly regulate nuclear androgen receptor signaling to drive tumorigenesis, thereby providing a link between aberrant metabolism and protumorigenic signaling in advanced prostate cancer. The findings from this study support exploring the GABA shunt, GAD65 in particular, as a molecular target in the treatment of CRPC.

Original languageEnglish
Pages (from-to)4580-4581
Number of pages2
JournalCancer Research
Volume79
Issue number18
DOIs
Publication statusPublished - 15 Sep 2019

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