Skip Navigation



Carcinogenesis Advance Access published online on February 12, 2004

Carcinogenesis, doi:10.1093/carcin/bgh106
© 2004 by Oxford University Press
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
25/7/1109    most recent
bgh106v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Lee, H.-H.
Right arrow Articles by Lin, J.-K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lee, H.-H.
Right arrow Articles by Lin, J.-K.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2004 Oxford University Press

CANCER BIOLOGY

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

Hung-Hsiao Lee 1, Chi-Tang Ho 2, and Jen-Kun Lin 1*

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

* Corresponding author. E-mail: jklin{at}ha.mc.ntu.edu.tw.

Received 16 September 2003 ; revised 3 January 2004 ; accepted 26 January 2004

Abstract

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 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-{beta}-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 androgen receptor (AR) and lowered androgen-induced prostate specific antigen (PSA) secretion and fatty acid synthase (FAS) protein level. In conclusion, our result suggests that TF3 and 5GG might be a useful chemoprevention agent for prostate cancer through suppressing the function of androgen and its receptor.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Molecular Cancer TherapeuticsHome page
H. Hu, H.-J. Lee, C. Jiang, J. Zhang, L. Wang, Y. Zhao, Q. Xiang, E.-O. Lee, S.-H. Kim, and J. Lu
Penta-1,2,3,4,6-O-galloyl-{beta}-D-glucose induces p53 and inhibits STAT3 in prostate cancer cells in vitro and suppresses prostate xenograft tumor growth in vivo
Mol. Cancer Ther., September 1, 2008; 7(9): 2681 - 2691.
[Abstract] [Full Text] [PDF]


Home page
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.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.