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Carcinogenesis Advance Access originally published online on March 11, 2004
Carcinogenesis 2004 25(8):1403-1408; doi:10.1093/carcin/bgh136
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Carcinogenesis vol.25 no.8 © Oxford University Press 2004; all rights reserved.

ARTICLE

Ingestion of an isothiocyanate metabolite from cruciferous vegetables inhibits growth of human prostate cancer cell xenografts by apoptosis and cell cycle arrest

Jen Wei Chiao1,4, Hongyan Wu1, Gita Ramaswamy1, C. Clifford Conaway2, Fung-Lung Chung2, Longgui Wang3 and Delong Liu1

1 Department of Medicine and Department of Pathology, New York Medical College, Valhalla, NY 10595, 2 Division of Carcinogenesis and Molecular Epidemiology, Institute for Cancer Prevention, Valhalla, NY 10595 and 3 Medical Oncology, Mount Sinai Medical Center, New York, NY 10029, USA

4 To whom correspondence should be addressed Email: jen-wei_chiao{at}nymc.edu

Epidemiological surveys indicate that intake of cruciferous vegetables is inversely related to prostate cancer incidence, although the responsible dietary factors have not been identified. Our studies demonstrated that exposure of human prostate cancer cells in culture to the N-acetylcysteine (NAC) conjugate of phenethyl isothiocyanate (PEITC-NAC), the major metabolite of PEITC that is abundant in watercress, inhibited proliferation and tumorigenesis. The PEITC-NAC is known to mediate cytoprotection at initiation of carcinogenesis. The relevance of PEITC-NAC in diets on the growth of prostate tumor cells has been evaluated in immunodeficient mice with xenografted tumors of human prostate cancer PC-3 cells. The daily PEITC-NAC (8 µmol/g) supplemented diet group showed a significant reduction in tumor size in 100% of the mice during the 9-week treatment period. Tumor weight at autopsy was reduced by 50% compared with mice on the diet without PEITC-NAC (P = 0.05). Mitosis and in vivo 5-bromo-2'-deoxyuridine labeled proliferating cells were reduced in these tumors. The PEITC-NAC diet up-regulated the inhibitors of cyclin-dependent kinases p21WAF-1/Cip-1 and p27Kip1, and reduced the expression of cyclins D and E, indicating they were potential molecular targets. As a result, phosphorylated Rb was significantly decreased and the G1- to S-phase transition retarded. The treated tumors also showed a significant increase in apoptosis as determined by in situ end-labeling, and by poly ADP-ribose polymerase cleavage. This study demonstrates the first in vivo evidence of dietary PEITC-NAC inhibiting tumorigenesis of prostate cancer cells. PEITC-NAC may prevent initiation of carcinogenesis and modulate the post-initiation phase by targeting cell cycle regulators and apoptosis induction.


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