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Allyl Isothiocyanate Induces Autophagy through the Up-Regulation of Beclin-1 in Human Prostate Cancer Cells.

Authors
  • Chen, Hung-En1
  • Lin, Ji-Fan2
  • Tsai, Te-Fu1, 3
  • Lin, Yi-Chia1, 3
  • Chou, Kuang-Yu1, 3
  • Hwang, Thomas I-Sheng1, 3, 4
  • 1 * Division of Urology, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan. , (Taiwan)
  • 2 † Central Laboratory, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan. , (Taiwan)
  • 3 ‡ Division of Urology, School of Medicine, Fu-Jen Catholic University, New Taipei 242, Taiwan. , (Taiwan)
  • 4 § Department of Urology, Taipei Medical University, Taipei 111, Taiwan. , (Taiwan)
Type
Published Article
Journal
The American journal of Chinese medicine
Publication Date
Oct 04, 2018
Pages
1–19
Identifiers
DOI: 10.1142/S0192415X18500830
PMID: 30284468
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Allyl isothiocyanate (AITC), one of the most widely studied phytochemicals, inhibits the survival of human prostate cancer cells while minimally affecting normal prostate epithelial cells. Our study demonstrates the mechanism of AITC-induced cell death in prostate cancer cells. AITC induces autophagy in RV1 and PC3 cells, judging from the increased level of LC3-II protein in a dose- and time-dependent manner, but not in the normal prostate epithelial cell (PrEC). Inhibition of autophagy in AITC-treated cells decreased cell viability and enhanced apoptosis, suggesting that the autophagy played a protective role. There are several pathways activated in ATIC-treated cells. We detected the phosphorylation forms of mTOR, ERK, AMPK, JNK and p38, and ERK AMPK and JNK activation were also detected. However, inhibition of AITC-activated ERK, AMPK and JNK by pre-treatment of specific inhibitors did not alter autophagy induction. Finally, increased beclin-1 expression was detected in AITC-treated cells, and inhibition of AITC-induced beclin-1 attanuated autophagy induction, indicating that AITC-induced autophagy occurs through upregulating beclin-1. Overall, our data show for the first time that AITC induces protective autophagy in Rv1 and PC3 cells through upregulation of beclin-1. Our results could potentially contribute to a therapeutic application of AITC in prostate cancer patients.

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