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The Neuroendocrine-Derived Peptide Parathyroid Hormone–Related Protein Promotes Prostate Cancer Cell Growth by Stabilizing the Androgen Receptor
Cancer Research, 09/18/09

DaSilva J et al. – PTHrP–induced tyrosine phosphorylation of AR resulted in reduced AR ubiquitination and interaction with the ubiquitin ligase COOH terminus of Hsp70–interacting protein. These events result in increased accumulation of AR and thus enhanced growth of prostate cancer cells at low levels of androgen.

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Sarah J. Parsons, 09/22/09

Prostate cancers usually require the Androgen Receptor even after they have progressed to become refractory to androgen ablation therapy. Progression of the disease is often accompanied by increased neuroendocrine differentiation that promotes aggressive growth through the production of paracrine growth factors. Before this study was undertaken, it had not been determined whether neuroendocrine-induced growth of prostate cancer is driven through an AR-dependent pathway or circumvents it. Here we provide evidence that the AR is involved in neuroendocrine effects. Our results show that neuroendocrine-derived PTHrP-mediated signaling increases intracellular AR levels by decreasing the rate of AR turnover, thus enabling prostate cancer cells to proliferate at reduced androgen concentrations.

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