Skip to main content
. Author manuscript; available in PMC: 2011 Nov 17.
Published in final edited form as: Cancer Cell. 2011 May 17;19(5):575–586. doi: 10.1016/j.ccr.2011.04.008

Figure 2. Inhibition of the PI3K pathway restores, in part, androgen responsive signaling in PTEN loss prostate cancers.

Figure 2

(A) AR protein levels by Western blot analysis in wild-type, Ptenlox/lox, and Ptenlox/lox mice treated with BEZ235. Ventral prostates from individual 8-week old mice were analyzed. (B) Western blot analysis of AR, pAKT, pS6, pERK in the LNCaP cell line treated for 24 hours with DMSO, BEZ235 (500nM), and RAD001 (100nM). (C) Expression analysis (qRT-PCR) of the androgen regulated genes Pbsn, Nkx3.1, and Psca in wild-type, Ptenlox/lox, and Ptenlox/lox mice treated with BEZ235, normalized to Hprt and wild-type intact mice. Ventral prostates from individual 8-week old mice were analyzed and mean fold-change +/− SD is reported. (D) Luciferase mean fold-change +/− SD measurements in the LNCaP AR-ARE-Luciferase cell line treated for 24 hours with DMSO, BEZ235 (500nM), RAD001 (100nM), and AKT1/2 inhibitor (1uM) normalized to DMSO. (E) Western blot analysis of HER2, HER3, AR, and PSA in the LNCaP cell line treated with DMSO and BEZ235 (500nM) for 24 hours and Ptenlox/lox mice treated with BEZ235. (F) Western blot analysis for HER3, AR, pAKT, pERK in LNCaP cells treated with BEZ235 or siRNA AKT1/2 for 24 hours. (G) Luciferase mean fold-change +/− SD measurements in the LNCaP AR-ARE-Luciferase cell line treated for 24 hours with DMSO, BEZ235 (500nM), RAD001 (100nM), with or without PKI166 (5uM) or PD0325901 (1uM) normalized to DMSO.