Capsaicin, a component of red peppers, induces expression of androgen receptor via PI3K and MAPK pathways in prostate LNCaP cells.

In this study, capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) induced an increase in the cell viability of the androgen-responsive prostate cancer LNCaP cells, which was reversed by the use of the TRPV1 antagonists capsazepine, I-RTX and SB 366791. In further studies we observed that capsaicin induced a decrease in ceramide levels as well as Akt and Erk activation. To investigate the mechanism of capsaicin action we measured androgen (AR) receptor levels. Capsaicin induced an increase in the AR expression that was reverted by the three TRPV1 antagonists. AR silencing by the use of siRNA, as well as blocking the AR receptor with bicalutamide, inhibited the proliferative effect of capsaicin.