Figure 4.

Matrine suppressed human prostate cancer cells by specifically activating the ER stress/UPR signaling pathway. The expression of key components of the PERK branch in the ER stress/UPR signaling pathway: (A) main target genes of ER stress/UPR mediating apoptosis; (B) the cell growth and (C) cell cycle, after DU 145 and PC-3 human prostate cancer cells were exposed to 4 mM matrine for 0–48 h; (D) the specific small-molecule chemical chaperone PBA could attenuate matrine-induced activation of the UPR/ER stress signaling pathway in human prostate cancer cells. The DU 145 and PC-3 prostate cancer cells were pretreated with PBA for 24 h before exposure to 4 mM matrine for another 24 h. Total proteins were extracted and western blotting was performed. β-Actin was used as a loading control. The data above are representative of three experiments with similar results. ER, endoplasmic reticulum; UPR, unfolded protein response; PBA, 4-phenylbutyric acid.