Carcinogenesis, Vol. 20, No. 7, 1185-1192,
July 1999
© 1999 Oxford University Press
Cancer Biology |
A human prostatic stromal myofibroblast cell line WPMY-1: a model for stromal–epithelial interactions in prostatic neoplasia
Departments of Zoology and Medicine, and
1 Department of Pediatrics and Human Development, Michigan State University, East Lansing, MI 48824-1312,
2 Department of Radiation Medicine, Georgetown University, Washington, DC,
3 Sparrow Regional Cancer Center, Lansing, MI and
4 Laboratory of Biochemical Physiology, National Cancer Institute, Frederick, MD, USA
Here we report the characterization of an SV40 large-T antigen-immortalized stromal cell line, WPMY-1, derived from the same prostate as our previously described epithelial cell lines. The WPMY-1 cells were determined to be myofibroblasts on the basis of co-expression of smooth muscle 
-actin and vimentin. They also show positive staining for androgen receptor, large-T antigen, and positive but heterogeneous staining for p53 and pRb. Their growth is stimulated by the synthetic androgen mibolerone to 145% of control (100%). Platelet-derived growth factor BB, epidermal growth factor and basic fibroblast growth factor, at 10 ng/ml, stimulated growth to 138, 143 and 146% of control, respectively. Transforming growth factor-ß, at 10 ng/ml, inhibited serum-induced growth to 65% of control in the presence of 1% serum, and bFGF-induced growth to 30% of control. A serum-free medium was developed for optimal growth of WPMY-1 cells. They show anchorage-independent growth in soft agar. Studies on paracrine interactions show that myofibroblast-conditioned medium causes a marked inhibition of growth in WPE1-10 cells, while conditioned medium from WPE1-10 prostatic epithelial cells caused only a small increase in the growth of WPMY-1 cells. WPMY-1 cells secrete very low levels of MMP-9 but high levels of MMP-2, markedly higher than the epithelial cells. These epithelial and myofibroblast cell lines, derived from the same prostate, provide novel and useful models for studies on paracrine stromal–epithelial interactions in carcinogenesis, tumor progression, prevention and treatment of prostate cancer and benign prostatic hyperplasia.
Abbreviations: -SMA, smooth muscle -actin; bFGF, basic fibroblast growth factor; BPH, benign prostate hyperplasia; EGF, epidermal growth factor; ITS, insulin–transferrin–selenium; MMPs, matrix metalloproteinases; MTT, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide; PDGF, platelet-derived growth factor; PSA, prostate specific antigen; TGF-ß, transforming growth factor ß.
5 To whom correspondence should be addressed Email: mwebber{at}pilot.msu.edu
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