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. 2011 May 23;108(23):9578–9582. doi: 10.1073/pnas.1106383108

Fig. 2.

Fig. 2.

Genetic and pharmacological inhibition of AR blocks androgen suppression of PSMA. (A) LNCaP and CWR22Rv1 (22Rv1) were transfected with nontargeted (NT) or AR-directed (AR) siRNA pools and treated with vehicle (EtOH) or DHT (10 nM). Whereas basal expression of PSMA is unaffected by AR knockdown in either cell line at this time point, AR silencing inhibits PSMA suppression by DHT, thus suggesting a role for AR in this process. Cells were transfected with 100 nM of siRNA, DHT challenge was initiated 24 h after transfection, and cells were harvested 48 h after androgen treatment. (B) Hormone withdrawal and antiandrogen treatment increase PSMA expression in LNCaP-AR in vitro. Cells were plated in media containing 10% (vol/vol) FBS and treated with vehicle, MDV3100 (10 μM), or the media was replaced with 10% (vol/vol) CSS (indicated as “-”). After 7 or 14 d, cells were harvested and incubated with Alexa Fluor 488-labeled J591, and PSMA expression was analyzed by FACS. Mean fluorescent intensities (MFI) were calculated and show that MDV3100 up-regulates PSMA expression by 7 d, whereas the effects of hormone withdrawal were observed between 7 and 14 d.