Skip Navigation



Carcinogenesis Advance Access published online on July 5, 2007
Carcinogenesis, doi:10.1093/carcin/bgm148
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
28/11/2282    most recent
bgm148v1
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 Chau, M. N.
Right arrow Articles by Banerjee, P. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chau, M. N.
Right arrow Articles by Banerjee, P. P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Physiologically Achievable Concentrations of Genistein Enhance Telomerase Activity in Prostate Cancer Cells via the Activation of STAT3

My N. Chau1, Lara H. El Touny1, Shankar Jagadeesh and Partha P. Banerjee*

Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, District of Columbia, USA

* Address all correspondence and request for reprints to: Partha P. Banerjee, Department of Biochemistry, Molecular and Cellular Biology, Medical-Dental Building, Room C406B, 3900 Reservoir Road, NW, Washington DC 20057, USA. Phone: (202)-687-8611; Fax: (202)-687-1823; E-mail: ppb{at}georgetown.edu.

Telomerase contributes to the infinite replicative potential of cancer cells by conferring proliferation and survival through the regulation of growth factors and apoptotic proteins. Although it is generally known that the phytoestrogen, genistein, has telomerase-repressing and anti-proliferative effects on various cancer cells at pharmacological concentrations, we report here that physiologically achievable concentrations of genistein enhance telomerase activity, the proliferation of human prostate cancer cells, and tumor growth in the Transgenic Adenocarcinoma Mouse Prostate (TRAMP) model. In determining the mechanism for enhanced telomerase activity, we observed that physiological concentrations of genistein activated STAT3 both in vitro and in vivo and increased STAT3 binding to the telomerase reverse transcriptase (TERT) promoter in human prostate cancer cells. These results demonstrate for the first time that physiologically achievable concentrations of genistein enhance TERT transcriptional activity in prostate cancer cells via the activation of STAT3. Consequently, these concentrations of genistein will augment the growth of prostate cancer cells which could be detrimental to individuals with prostate cancer and therefore, caution should be exercised when genistein is considered for chemotherapeutic purposes.

Key Words: Genistein • Prostate cancer • STAT3 • Telomerase • TERT • TRAMP

Grant support: This work was supported by NIH grant R01 DK060875 to Partha P. Banerjee.

1 These authors contributed equally

Received February 23, 2007; revised June 19, 2007; accepted June 22, 2007.


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




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.