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Carcinogenesis Advance Access originally published online on June 13, 2006
Carcinogenesis 2006 27(11):2223-2234; doi:10.1093/carcin/bgl087
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential

Dong Xiao, Karen L. Lew, Yan Zeng, Hui Xiao, Stanley W. Marynowski, Rajiv Dhir and Shivendra V. Singh*

Departments of Pharmacology and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine Pittsburgh, PA, USA

*To whom correspondence should be addressed. Tel: +1 412 623 3263; Fax: +1 412 623 7828; E-mail: singhs{at}upmc.edu

The present study was undertaken to gain insights into the molecular mechanism of apoptosis induction by phenethyl isothiocyanate (PEITC), which is a cancer chemopreventive constituent of cruciferous vegetables, using PC-3 human prostate cancer cells as a model. The PEITC-induced cell death in PC-3 cells was associated with disruption of the mitochondrial membrane potential, release of apoptogenic molecules (cytochrome c and Smac/DIABLO) from mitochondria to the cytosol and generation of reactive oxygen species (ROS), which were blocked in the presence of a combined mimetic of superoxide dismutase and catalase (Euk134). Ectopic expression of Bcl-xL, whose protein level is reduced markedly on treatment of PC-3 cells with PEITC, conferred partial protection against PEITC-induced apoptosis only at higher drug concentrations (>10 µM). Administration of 12 µmol PEITC/day (Monday through Friday) by oral gavage significantly retarded growth of PC-3 xenografts in athymic mice. For instance, 31 days after the initiation of PEITC administration, the average tumor volume in control mice (721 ± 153 mm3) was ~2-fold higher compared with mice receiving 12 µmol PEITC/day. The PEITC-mediated inhibition of PC-3 xenograft growth was associated with induction of Bax and Bid proteins. In conclusion, the present study indicates that the PEITC-induced apoptosis in PC-3 cells is mediated by ROS-dependent disruption of the mitochondrial membrane potential and regulated by Bax and Bid.


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