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Article

ß-Carotene Modulates Human Prostate Cancer Cell Growth and May Undergo Intracellular Metabolism to Retinol^{1 ,2 ,3}

Alexa W. Williams^*, Thomas W.-M. Boileau^*, Jin Rong Zhou, Steven K. Clinton^** and John W. Erdman, Jr.^*4

^* Division of Nutritional Sciences and Department of Food Science and Human Nutrition, University of Illinois, Urbana-Champaign, IL 61801; Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215; and ^** Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Division of Hematology and Oncology, The Ohio State University, Columbus, OH 43210-1240

⁴To whom correspondence should be addressed.

Epidemiologic and animal studies provide support for a relationship between high intakes of carotenoids from fruits and vegetables with reduced risk of several malignancies including prostate cancer. The highly controlled environments of in vitro systems provide an opportunity to investigate the cellular and molecular effects of carotenoids. The effects of ß-carotene (BC) on in vitro growth rates, p21^WAF1 and p53 gene expression, as well as the conversion of BC to retinol were investigated in three human prostate adenocarcinoma cell lines: PC-3, DU 145 and LNCaP. In these experiments, media concentrations of 30 µmol BC/L for 72 h significantly (P < 0.05) slowed in vitro growth rates in all three cell lines, independently of p53 or p21^WAF1 status or expression. ¹⁴C-labeled retinol was detected in prostate tumor cells incubated with ¹⁴C-labeled BC, suggesting metabolic conversion of BC to retinol. Conversely, no ¹⁴C-labeled retinol was detected in media incubated without prostate cancer cells. These studies support a hypothesis that in vitro biological effects of BC on prostate cells may result in part from the conversion of BC to retinol or other metabolites. The possibility that prostate cancer cells in vivo locally metabolize provitamin A carotenoids to retinol and other related metabolites may have implications for our understanding of prostate cancer etiology and the design of future prevention studies.

KEY WORDS: • prostate cancer • ß-carotene • vitamin A • retinoids • cell culture

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