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Carcinogenesis Advance Access originally published online on April 15, 2008
Carcinogenesis 2008 29(6):1134-1138; doi:10.1093/carcin/bgn097
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Glutathione S-transferase Pi mediates proliferation of androgen-independent prostate cancer cells

Naomi Hokaiwado1,2, Fumitaka Takeshita2, Aya Naiki-Ito1, Makoto Asamoto1,*, Takahiro Ochiya2 and Tomoyuki Shirai1

1 Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan
2 Section for Studies on Metastasis, National Cancer Center Research Institute, Tokyo 104-0045, Japan

* To whom correspondence should be addressed. Tel: +81 52 853 8156; Fax: +81 52 841 0817; Email: masamoto{at}med.nagoya-cu.ac.jp

Prostate cancers generally acquire an androgen-independent growth capacity with progression, resulting in resistance to antiandrogen therapy. Therefore, identification of the genes regulated through this process may be important for understanding the mechanisms of prostate carcinogenesis. We here utilized androgen-dependent/independent transplantable tumors, newly established with the ‘transgenic rat adenocarcinoma in prostate’ (TRAP) model, to analyze their gene expression using microarrays. Among the overexpressed genes in androgen-independent prostate cancers compared with the androgen-dependent tumors, glutathione S-transferase pi (GST-pi) was included. In line with this, human prostate cancer cell lines PC3 and DU145 (androgen independent) had higher expression of GST-pi compared with LNCaP (androgen dependent) as determined by semiquantitative reverse transcription–polymerase chain reaction analysis. To investigate the roles of GST-pi expression in androgen-independent human prostate cancers, GST-pi was knocked down by a small interfering RNA (siRNA), resulting in significant decrease of the proliferation rate in the androgen-independent PC3 cell line. In vivo, administration of GST-pi siRNA–atelocollagen complex decreased GST-pi protein expression, resulting in enhanced numbers of TdT mediated dUTP-biotin nick-end labering (TUNEL)-positive apoptotic cells. These findings suggest that GST-pi might play important roles in proliferation of androgen-independent human prostate cancer cells.

Abbreviations: AR, androgen receptor; GST-pi, glutathione S-transferase pi; mRNA, messenger RNA; PC3ML, PC3M-luc-C6; siRNA, small interfering RNA; TRAP, transgenic rat adenocarcinoma in prostate

Received December 1, 2007; revised April 2, 2008; accepted April 8, 2008.


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