In conclusion, our study demonstrated that BP 1) causes prostate cancer cell cycle arrest at G0/G1 phase by targeting the Akt-GSK-3β-Cyclin D1 signaling axis; 2) induces cell death via ER-stress- and JNK-mediated UPR; 3) triggers apoptosis of human prostate cancer cells through multiple apoptotic pathways in vitro and in vivo (Fig. 9). This evidence concerns the gene AKT1 and prostate carcinoma.