β-Carotene Modulates Human Prostate Cancer Cell Growth and May Undergo Intracellular Metabolism to Retinol

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 cel...

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Bibliographic Details
Published in:The Journal of nutrition 2000-04, Vol.130 (4), p.728-732
Main Authors: Williams, Alexa W., Boileau, Thomas W.-M., Zhou, Jin Rong, Clinton, Steven K., Erdman, John W.
Format: Article
Language:English
Subjects:
Adenocarcinoma - metabolism
Adenocarcinoma - pathology
beta Carotene - metabolism
beta Carotene - pharmacology
beta Carotene - physiology
Biological and medical sciences
cell culture
Cell Division - physiology
Cyclin-Dependent Kinase Inhibitor p21
Cyclins - metabolism
Gynecology. Andrology. Obstetrics
Humans
Intracellular Fluid - metabolism
Male
Male genital diseases
Medical sciences
Metabolism
Nutrition
Prevention
Prostate cancer
Prostatic Neoplasms - metabolism
Prostatic Neoplasms - pathology
retinoids
Tumor Cells, Cultured - drug effects
Tumor Cells, Cultured - pathology
Tumor Suppressor Protein p53 - metabolism
Tumors
Vitamin A
Vitamin A - biosynthesis
β-carotene
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Summary: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 β-carotene (BC) on in vitro growth rates, p21WAF1 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 p21WAF1 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.
ISSN:0022-3166
1541-6100
DOI:10.1093/jn/130.4.728