Autophagy inhibition enhances silibinin-induced apoptosis by regulating reactive oxygen species production in human prostate cancer PC-3 cells

Sang Hun Kim, Kwang Youn Kim, Sun Nyoung Yu, Seul Ki Park, Hyeun Deok Choi, Jae Hoon Ji, Soon Cheol Ahn

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)151-156
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume468
Issue number1-2
DOIs
StatePublished - Dec 4 2015
Externally publishedYes

Keywords

  • Apoptosis
  • Autophagy
  • PC-3 cells
  • Reactive oxygen species
  • Silibinin

ASJC Scopus subject areas

  • Molecular Biology
  • Biophysics
  • Biochemistry
  • Cell Biology

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