In BK virus (BKV)/tat transgenic mice, the relatively low incidence and long latency period of tumors indicate that the BKV/tat transgene is not sufficient for the expression of a complete oncogenic phenotype. Since angiogenesis and the production of proteases are critical for tumor growth, we evaluated the expression of two potent angiogenic molecules, fibroblast growth factor type 2 (FGF-2), and hepatocyte growth factor (HGF), and of the fibrinolytic system in cell lines isolated from tumors of different histotypes developed by BKV/tat transgenic mice. Here we show that the overexpression of HGF is a unique feature of spindle cells derived from murine Kaposi's sarcoma-like lesions, whereas FGF-2 is detectable in all the cell lines tested. Interestingly, FGF-2 is secreted only by adenocarcinoma-derived T53 cells that show a fully transformed phenotype in vitro. In addition, T53 cells synthesize larger amounts of urokinase-type plasminogen activator (uPA) than the other cell lines studied. This is due to the secretion of FGF-2 and not to the presence of extracellular Tat. We conclude that the high levels of expression of uPA and its receptor, and the very low levels of plasminogen activator inhibitor type 1, may contribute to the tumorigenic phenotype of T53 cells.
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