Erythropoietin stimulates growth and STAT5 phosphorylation in human prostate epithelial and prostate cancer cells
Article first published online: 13 SEP 2005
Copyright © 2005 Wiley-Liss, Inc.
Volume 66, Issue 2, pages 135–145, 1 February 2006
How to Cite
Feldman, L., Wang, Y., Rhim, J. S., Bhattacharya, N., Loda, M. and Sytkowski, A. J. (2006), Erythropoietin stimulates growth and STAT5 phosphorylation in human prostate epithelial and prostate cancer cells. Prostate, 66: 135–145. doi: 10.1002/pros.20310
- Issue published online: 9 DEC 2005
- Article first published online: 13 SEP 2005
- Manuscript Accepted: 1 JUN 2005
- Manuscript Received: 13 DEC 2004
- William F. Milton Foundation
- DOD. Grant Numbers: DAMD17-03-1-0173, DAMD17-02-1-0014
- NIH. Grant Numbers: R01 CA89204, R03 CA96047
- American Institute for Cancer Research
- erythropoietin receptor;
- prostate cancer;
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.
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.
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.
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.