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Carcinogenesis Advance Access originally published online on July 5, 2007
Carcinogenesis 2007 28(11):2282-2290; doi:10.1093/carcin/bgm148
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© 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. Chau{dagger}, Lara H. El Touny{dagger}, Shankar Jagadeesh and Partha P. Banerjee*

Department of Biochemistry and Molecular and Cellular Biology, Medical-Dental Building, Georgetown University Medical Center, 3900 Reservoir Road, NW, Washington, DC 20057, USA

* To whom correspondence should be addressed. Tel: +202 687 8611; Fax: +202 687 1823; Email: 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 model. In determining the mechanism for enhanced telomerase activity, we observed that physiological concentrations of genistein activated signal transducers and activators of transcription 3 (STAT3) both in vitro and in vivo and increased STAT3 binding to the telomerase reverse transcriptase promoter in human prostate cancer cells. These results demonstrate for the first time that physiologically achievable concentrations of genistein enhance telomerase reverse transcriptase transcriptional activity in prostate cancer cells via the activation of STAT3. Consequently, these concentrations of genistein will augment the growth of prostate cancer cells that could be detrimental to individuals with prostate cancer and therefore, caution should be exercised when genistein is considered for chemotherapeutic purposes.

Abbreviations: DLPs, dorsolateral prostates; TERT, telomerase reverse transcriptase; mRNA, messenger RNA; PCR, polymerase chain rection; PrECs, prostate epithelial cells; PIN, prostatic intraepithelial neoplasia; RT, reverse transcriptase; STAT, signal transducers and activators of transcription; siRNA, small interfering RNA; TEP1, telomerase-associated protein 1; TERC, telomerase RNA; TRAP, telomeric repeat amplification protocol; TRAMP, transgenic adenocarcinoma mouse prostate

{dagger} These authors contributed equally to this work.

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


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