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Erythropoietin stimulates growth and STAT5 phosphorylation in human prostate epithelial and prostate cancer cells
Author(s) -
Feldman Laurie,
Wang Yuxun,
Rhim Johng S.,
Bhattacharya Nandita,
Loda Massimo,
Sytkowski Arthur J.
Publication year - 2006
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20310
Subject(s) - erythropoietin receptor , prostate cancer , erythropoietin , stat5 , cancer research , prostate , biology , cell growth , cancer cell , medicine , cancer , phosphorylation , endocrinology , microbiology and biotechnology , genetics
BACKGROUND Erythropoietin (Epo), the principal regulator of erythroid progenitor survival, growth, and differentiation, initiates its action by binding to its cognate cell surface receptor (EpoR). EpoR have been identified on a variety of non‐hematopoietic cells, both normal and malignant, however, little is known about the function of EpoR on malignant cells. METHODS RT‐PCR, Western blotting, and immunohistochemistry were used to demonstrate that prostate cancer cells express EpoR at both the gene and protein level. Cell proliferation assays and STAT5 phosphorylation were used to demonstrate Epo's mitogenic action and intracellular signaling, respectively. RESULTS We have demonstrated that transformed prostate epithelial and prostate cancer cell lines, as well as primary prostate tissue, express the EpoR. Importantly, the EpoR on prostate cells are functional, as demonstrated by the observation that each of the cell lines exhibited a dose‐dependent proliferative response to Epo, and that Epo triggered STAT5b phosphorylation in the cells. CONCLUSION Human prostatic epithelial cells and prostate cancer cells express functional EpoR, and Epo serves as a growth factor for these cells. These results have implications for our understanding of normal prostatic growth and development and of the pathobiology of human prostate cancer. © 2005 Wiley‐Liss, Inc.