The importance of stromal-epithelial cell interaction in prostate tumorigenesis is well established. Many factors, including the members of the TGF beta protein family, are involved in the interactions. Upon knocking out the TGF beta type II receptor in fibroblasts in mice (FßIIKO), fibroblastic hyperplasia, accompanied by pre-neoplastic PIN (prostatic intraepithelial neoplasia) lesions in epithelial cells, were observed where c-myc oncogene expression was elevated in both fibroblast and epithelial cells. Thus we hypothesized that over-expression of c-myc in stromal fibroblasts mediates the developments of PIN lesions in FßIIKO mice. We demonstrated that cell proliferation is elevated in prostate fibroblasts (PF) over-expressing c-myc (myc-PF) compared to both wild type (wt-PF) and FßIIKO (KO-PF) cells. In contrast to wt-PF, myc-PF and KO-PF were found to proliferate in an androgen-independent manner in vitro. In vivo experiments recombining wild type prostatic epithelial cells with (wt- or myc-) fibroblasts in a xenograft model demonstrated that the prostatic graft from the myc-PF was not different from the wt-PF graft morphologically. However, there were more epithelial proliferative and apoptotic cells in the grafts containing myc-PF, compared to those containing wt-PF cells. This suggests that the c-myc expression in the fibroblasts was likely part of the reason that the FßIIKO prostate developed PIN.

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