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Carcinogenesis Advance Access originally published online on February 12, 2004
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Carcinogenesis, Vol. 25, No. 7, 1109-1118, July 2004
Carcinogenesis vol.25 no.7 © Oxford University Press 2004; all rights reserved.

ARTICLE

Theaflavin-3,3'-digallate and penta-O-galloyl-ß-D-glucose inhibit rat liver microsomal 5{alpha}-reductase activity and the expression of androgen receptor in LNCaP prostate cancer cells

Hung-Hsiao Lee1, Chi-Tang Ho2 and Jen-Kun Lin1,3

1 Institute of Biochemistry, College of Medicine, National Taiwan University, Taipei, Taiwan and 2 Department of Food Science, Rutgers University, Brunswick, New Jersey, USA

3 To whom correspondence should be addressed Email: jklin{at}ha.mc.ntu.edu.tw

Androgens play a critical role in regulating the growth, differentiation and survival of epithelial cells in many androgen-responsive organs, such as prostate and skin. The enzyme steroid 5{alpha}-reductase (EC 1.3.99.5) catalyzes the conversion of testosterone (T) to a more active androgen, dihydrotestosterone (DHT). DHT then binds to androgen receptors (AR) and functions in the nucleus to regulate specific gene expression. Androgens via their cognate receptor may be involved in the development and progression of benign prostate hyperplasia, prostate cancer, hirsutism, male pattern alopecia and acne. The aim of this study was to determine whether theaflavin-3,3'-digallate (TF3) and penta-O-galloyl-ß-D-glucose (5GG) have inhibitory effects on androgen production and action. We found that TF3 and 5GG inhibit rat liver microsomal 5{alpha}-reductase activity. Furthermore, TF3 and 5GG significantly reduced androgen-responsive LNCaP prostate cancer cell growth, suppressed expression of the AR and lowered androgen-induced prostate-specific antigen secretion and fatty acid synthase protein level. In conclusion, our result suggests that TF3 and 5GG might be useful chemoprevention agents for prostate cancer through suppressing the function of androgen and its receptor.


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 Endocr Relat CancerHome page
R. P Singh and R. Agarwal
Mechanisms of action of novel agents for prostate cancer chemoprevention.
Endocr. Relat. Cancer, September 1, 2006; 13(3): 751 - 778.
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