Silibinin is a major bioactive component of
silymarin and has anticancer effects on
cancer cell line and has been used as a supportive
therapy for chronic inflammatory liver condition. These anticancer effects of
silibinin have been demonstrated both in vitro and in vivo
cancer models. Although various evidences showed apoptosis signaling pathways by
silibinin, there is no report to address the clearly mechanism of
silibinin-induced autophagy in
prostate cancer PC-3 cells. Our study showed that
silibinin triggered autophagy through up-regulation of
microtubule-associated protein 1 light chain 3 (LC3)-II, formation of acidic vesicular organelles (AVO) and punctuate of GFP-LC3, which was inhibited by
3-methyladenine (3-MA), an inhibitor of specific autophagy. In addition,
silibinin induced autophagy through production of
reactive oxygen species (ROS). Inhibition of ROS with
diphenyleneiodonium (DPI), a ROS inhibitor, attenuated
silibinin-triggered autophagy. Inhibition of autophagy with 3-MA enhanced the
silibinin-induced apoptosis through the regulation of
caspase-3 and PARP. These results suggested that
silibinin induced autophagy by regulating ROS and its mechanism played a protective role against apoptosis in PC-3 cells.