JME
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Journal of Molecular Endocrinology (2006) 37 283-300    DOI: 10.1677/jme.1.02062
© 2006 Society for Endocrinology
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (3)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhou, L.
Right arrow Articles by Wang, Z.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhou, L.
Right arrow Articles by Wang, Z.

Roles of the androgen receptor cofactor p44 in the growth of prostate epithelial cells

Liran Zhou*, Hong Wu*, Peng Lee1 and Zhengxin Wang

Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard-173, Houston, Texas 77030, USA
1 Department of Pathology, New York University School of Medicine, New York, New York 10010, USA

(Requests for offprints should be addressed to Z Wang; Email: zhenwang{at}mdanderson.org)

* (L Zhou and H Wu contributed equally to this work)

Various cofactors have been shown to regulate androgen receptor (AR) transactivation, but their physiological functions in the AR pathway and prostate tumorigenesis are undefined. Here, we found that AR cofactor (p44) translocation from the nucleus to the cytoplasm in prostate epithelial cells (ECs) is associated with prostate tumorigenesis. The forced nuclear localization of p44 inhibited prostate cancer cell growth by G1 cell-cycle arrest. Consistently, mice lacking one allele of the p44 gene developed prostatic hyperplasia. Therefore, p44 is required for proper expression of AR-target genes to maintain the differentiation of prostate ECs, and p44 translocation from the nucleus into the cytoplasm in prostate cancer cells or loss of one allele in mouse results in excessive prostate EC proliferation.




This article has been cited by other articles:


Home page
 Cancer Res.Home page
Y. Li, L. Wang, M. Zhang, J. Melamed, X. Liu, R. Reiter, J. Wei, Y. Peng, X. Zou, A. Pellicer, et al.
LEF1 in Androgen-Independent Prostate Cancer: Regulation of Androgen Receptor Expression, Prostate Cancer Growth, and Invasion
Cancer Res., April 15, 2009; 69(8): 3332 - 3338.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
S. I. Park, J. Zhang, K. A. Phillips, J. C. Araujo, A. M. Najjar, A. Y. Volgin, J. G. Gelovani, S.-J. Kim, Z. Wang, and G. E. Gallick
Targeting Src Family Kinases Inhibits Growth and Lymph Node Metastases of Prostate Cancer in an Orthotopic Nude Mouse Model
Cancer Res., May 1, 2008; 68(9): 3323 - 3333.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
Y. Peng, F. Chen, J. Melamed, L. Chiriboga, J. Wei, X. Kong, M. Mcleod, Y. Li, C. X. Li, A. Feng, et al.
Distinct nuclear and cytoplasmic functions of androgen receptor cofactor p44 and association with androgen-independent prostate cancer
PNAS, April 1, 2008; 105(13): 5236 - 5241.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the Society for Endocrinology.