Skip Navigation



Carcinogenesis Advance Access published online on May 17, 2007
Carcinogenesis, doi:10.1093/carcin/bgm120
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
28/8/1752    most recent
bgm120v1
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 Kikuchi, H.
Right arrow Articles by Kitagawa, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kikuchi, H.
Right arrow Articles by Kitagawa, M.
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

ARA54 is involved in transcriptional regulation of the cyclin D1 gene in human cancer cells

Hirotoshi Kikuchi1,2, Chiharu Uchida2, Takayuki Hattori2, Tomoyasu Isobe1, Yoshihiro Hiramatsu1,2, Kyoko Kitagawa2, Toshiaki Oda2, Hiroyuki Konno1 and Masatoshi Kitagawa2

1 Second Department of Surgery 1, Hamamatsu University School of Medicine, Hamamatsu, Japan
2 Department of Biochemistry 1, Hamamatsu University School of Medicine, Hamamatsu, Japan

Requests for reprints: Masatoshi Kitagawa, Department of Biochemistry 1, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu 431-3192, Japan. Phone: +81-53-435-2322; Fax: +81-53-435-2322; E-mail: kitamasa{at}hama-med.ac.jp

Cyclin D1 is one of the major enhancers of cell cycle progression and its expression is regulated in several growth stimulatory signaling pathways. ARA54 is an androgen receptor (AR) co-activator that enhances AR-dependent transcriptional activation. Although expression of ARA54 mRNA is observed in a variety of human tissues at low levels, the AR- or androgen-independent function of ARA54 in those tissues remains unclear. In this study we identified a novel role for ARA54 in the regulation of cyclin D1 expression in the absence of AR stimulation in human cancer cells. Depletion of endogenous ARA54 by small interfering RNA decreased both the protein and mRNA levels of cyclin D1. These changes did not result from a reduction in the half-life of either the protein or the mRNA, but from suppression of cyclin D1 gene transcription. In T98G cells, depletion of ARA54 increased the population of cells in G1 phase, but reduced the population of cells in S phase, leading to a significant increase in the G1/S ratio and impaired cell growth. Furthermore, the amount of ARA54 mRNA appeared to positively correlate with cyclin D1 mRNA levels in specimens of clinical colon carcinomas, indicating that ARA54 is not only involved in the regulation of cyclin D1 expression in cultured cell lines, but also in clinical cancer specimens. These results suggest that ARA54 might participate in enhancing cell cycle progression and cell proliferation via induction of cyclin D1.

Received February 21, 2007; revised April 25, 2007; accepted May 12, 2007.


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
 Cancer Res.Home page
M. Yamamoto, H. Kikuchi, M. Ohta, T. Kawabata, Y. Hiramatsu, K. Kondo, M. Baba, K. Kamiya, T. Tanaka, M. Kitagawa, et al.
TSU68 Prevents Liver Metastasis of Colon Cancer Xenografts by Modulating the Premetastatic Niche
Cancer Res., December 1, 2008; 68(23): 9754 - 9762.
[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.