Pharmaceutical Sciences Faculty Publications
Regulation of Androgen Receptor Activity by Tyrosine Phosphorylation
Document Type
Article
Publication Date
10-1-2006
Journal Title
Cancer Cell
ISSN
1535-6108
Volume
10
Issue
4
First Page
309
Last Page
319
DOI
10.1016/j.ccr.2006.08.021
PubMed ID
17045208
Abstract
The androgen receptor (AR) is essential for the growth of prostate cancer cells. Here, we report that tyrosine phosphorylation of AR is induced by growth factors and elevated in hormone-refractory prostate tumors. Mutation of the major tyrosine phosphorylation site in AR significantly inhibits the growth of prostate cancer cells under androgen-depleted conditions. The Src tyrosine kinase appears to be responsible for phosphorylating AR, and there is a positive correlation of AR tyrosine phosphorylation with Src tyrosine kinase activity in human prostate tumors. Our data collectively suggest that growth factors and their downstream tyrosine kinases, which are elevated during hormone-ablation therapy, can induce tyrosine phosphorylation of AR and such modification may be important for prostate tumor growth under androgen-depleted conditions.
Keywords
Androgens, cell line, tumor, chlorocebus aethiops, dihydrotestosterone, epidermal growth factor, gene expression regulation, neoplastic, immunohistochemistry, indoles, kinetics, phosphorylation, prostatic neoplasms, pyrimidines, receptors, sulfonamides, tyrosine
Recommended Citation
Guo, Zhiyong; Dai, Bojie; Jiang, Tianyun; Xu, Kexin; Xie, Yingqiu; Kim, Oekyung; Nesheiwat, Issa; Kong, Xiangtian; Melamed, Jonathan; Handratta, Venkatesh D.; Njar, Vincent C.O.; Brodie, Angela M.H.; Yu, Li-Rong; Veenstra, Timothy D.; Chen, Hegang; and Qiu, Yun, "Regulation of Androgen Receptor Activity by Tyrosine Phosphorylation" (2006). Pharmaceutical Sciences Faculty Publications. 390.
https://digitalcommons.cedarville.edu/pharmaceutical_sciences_publications/390
