GPR30-targeted therapy with G-1 in CRPC

Lam and colleagues demonstrate that G-1, a GPR30 agonist, inhibits the growth of castration-resistant prostate cancer tumours, but not during the androgen-sensitive growth phase. The G-1-induced growth inhibitory response was manifested as massive necrosis attended by marked neutrophil infiltration in the affected tumours, associated with the activation of gene pathways involved in innate antitumor immunity. They also demonstrate that androgen suppressed GPR30 expression in an AR-dependent manner, and that castration markedly upregulated GPR30 expression. Clinically, they observed an elevated prevalence of GPR30 in CRPC metastases when compared with that of primary prostate cancer.  These findings provide evidence for the effective preclinical targeting of GPR30 with G-1 in CRPC.

Read the full article at Lam et al. (2014) Endocrine-Related Cancer 21 903–914 DOI:10.1530/ERC-14-0402