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The androgen receptor coordinates biosynthesis and proliferation in prostate cancer

ABSTRACT: The androgen receptor (AR) is the major therapeutic target in prostate cancer, although the important targets of the AR have remained obscure. Here we report a detailed genomic profile of AR signalling and find that the AR directly regulates glycolysis, anabolic metabolism and cell cycle regulators in prostate cancer. This coordinated transcriptional program promotes cancer cell proliferation and enhances the macromolecular synthesis needed to produce daughter cells. Clinical gene expression profiles and mechanistic studies highlight the importance of CAMKK2, an AR target which regulates both cell proliferation and metabolism. Thus our genomics study identifies a direct link between AR signalling and aerobic glycolysis (the Warburg effect), providing a new perspective on the oncogenic function of the AR in prostate cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28126 | GEO | 2011/03/24

SECONDARY ACCESSION(S): PRJNA139851

REPOSITORIES: GEO

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The androgen receptor coordinates biosynthesis and proliferation in prostate cancer

Project description:The androgen receptor (AR) is the major therapeutic target in prostate cancer, although the important targets of the AR have remained obscure. Here we report a detailed genomic profile of AR signalling and find that the AR directly regulates glycolysis, anabolic metabolism and cell cycle regulators in prostate cancer. This coordinated transcriptional program promotes cancer cell proliferation and enhances the macromolecular synthesis needed to produce daughter cells. Clinical gene expression profiles and mechanistic studies highlight the importance of CAMKK2, an AR target which regulates both cell proliferation and metabolism. Thus our genomics study identifies a direct link between AR signalling and aerobic glycolysis (the Warburg effect), providing a new perspective on the oncogenic function of the AR in prostate cancer. 8 Samples: Chromatin IP using AR and PolII in stimulated and unstimulated LNCaP and VCaP cells.

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Schlafen family member 5 (SLFN5) regulates LAT1-mediated mTOR activation in castration-resistant prostate cancer (PART 1)

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