Prostate-specific G-protein-coupled receptor collaborates with loss of PTEN to promote prostate cancer progression.

ABSTRACT: Among frequent events in prostate cancer are loss of the tumor-suppressor phosphatase and tensin homologue (PTEN) and overexpression of prostate-specific G-protein-coupled receptor (PSGR), but the potential tumorigenic synergy between these lesions is unknown. Here, we report a new mouse model (PSGR-Pten(Δ/Δ)) combining prostate-specific loss of Pten with probasin promoter-driven PSGR overexpression. By 12 months PSGR-Pten(Δ/Δ) mice developed invasive prostate tumors featuring Akt activation and extensive inflammatory cell infiltration. PSGR-Pten(Δ/Δ) tumors exhibited E-cadherin loss and increased stromal androgen receptor (AR) expression. PSGR overexpression increased LNCaP proliferation, whereas PSGR short hairpin RNA knockdown inhibited proliferation and migration. In conclusion, we dem

SUBMITTER: Rodriguez M 

PROVIDER: S-EPMC4683109 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature