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Carcinogenesis Advance Access published online on March 11, 2004
Carcinogenesis, doi:10.1093/carcin/bgh136
© 2004 by Oxford University Press
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© 2004 Oxford University Press

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

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

Jen Wei Chiao 1*, Hongyan Wu 1, Gita Ramaswamy 1, C. Clifford Conaway 2, Fung-Lung Chung 2, Longgui Wang 3, and Delong Liu 1

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

* Corresponding author. E-mail: Jen-Wei_Chiao{at}NYMC.edu.

Received 4 November 2003 ; revised 19 February 2004 ; accepted 27 February 2004

Abstract

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 nine-week treatment period. Tumor weight at autopsy was reduced by 50% compared with mice on diet without PEITC-NAC (P=0.05). Mitosis and in vivo BrdU 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 PARP 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 postinitiation phase by targeting cell cycle regulators and apoptosis induction.


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