Regulation of androgen receptor activity by tyrosine phosphorylation

Zhiyong Guo, Bojie Dai, Tianyun Jiang, Kexin Xu, Yingqiu Xie, Oekyung Kim, Issa Nesheiwat, Xiangtian Kong, Jonathan Melamed, Venkatesh D. Handratta, Vincent C.O. Njar, Angela M.H. Brodie, Li Rong Yu, Timothy D. Veenstra, Hegang Chen, Yun Qiu

Research output: Contribution to journalArticlepeer-review

284 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)309-319
Number of pages11
JournalCancer Cell
Issue number4
StatePublished - Oct 2006
Externally publishedYes



ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research


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