Based on the results of the present study, we propose that VNPP433-3β exerts the antitumor effect by imposing (1) transcriptional regulation of AR and AR-responsive oncogenes via degrading AR, (2) translational regulation by depleting Mnk1/2 thereby impeding phosphorylation of eIF4E and subsequent mRNA-5′cap-dependent translation initiation, (3) reducing AR half-life through enhanced proteasomal degradation and (4) modulating transcription of several genes relevant to PCa. This evidence concerns the gene MKNK1 and posterior cortical atrophy.