ARA55 is both an AR coactivator and a focal adhesion protein (Hic-5). Its role in the progression of prostate carcinoma may therefore involve these two different functions. Its decrease in cancer tissue suggests that it plays a different role than that expected, namely, facilitate cell proliferation and therefore mobility and metastasis.

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BACKGROUND Stromal–epithelial interactions play a critical role in prostate development, but the precise mechanisms are still unknown. Transforming growth factor‐beta (TGFβ) could be a potential mediator of these interactions, but there is as yet no clear demonstration of its role. METHODS Separate cultures and co‐cultures of fibroblasts and epithelial human prostate cells were performed. We measured TGFβ1 and TGFβ2 secretion by specific ELISA assay, cell growth by DNA assay, and TGFβ type II receptor expression by RT‐PCR. RESULTS Co‐culture resulted in a 20% inhibition of epithelial cell growth, similar to that obtained after TGFβ treatment (2 ng/ml for 48 hr), but without affecting fibroblast proliferation. This was accompanied by a five‐ to six‐fold increase in epithelial TGFβ2 secretion. CONCLUSIONS These results demonstrate for the first time that TGFβ2 secretion by prostate epithelial cells is under the direct control of a diffusible factor secreted by fibroblasts. They emphasize the role of TGFβ in stromal–epithelial interactions. Prostate 46:311–318, 2001. © 2001 Wiley‐Liss, Inc.