Author/Authors :
Guo، نويسنده , , Zhiyong and Dai، نويسنده , , Bojie and Jiang، نويسنده , , Tianyun and Xu، نويسنده , , Kexin and Xie، نويسنده , , Yingqiu and Kim، نويسنده , , Oekyung and Nesheiwat، نويسنده , , Issa and Kong، نويسنده , , Xiangtian and Melamed، نويسنده , , Jonathan and Handratta، نويسنده , , Venkatesh D. and Njar، نويسنده , , Vincent C.O. and Brodie، نويسنده , , Angela M.H. and Yu، نويسنده , , Li-Rong and Veenstra، نويسنده , , Timothy D. and Chen، نويسنده , , Hegang and Qiu، نويسنده , , Yun، نويسنده ,
Abstract :
Summary
drogen 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.
