Over-expression of components of the urokinase system is well documented in cancer and is thought to enable tumour cells to migrate and invade. Changes in integrin expression are also a common feature of tumours and have been linked to changes in protease activity. It has been shown that the *vÎ²6 integrin is neo-expressed in a number of epithelial carcinomas and in wound healing situations. We therefore investigated whether *vÎ²6 is able to modulate a key regulator of proteolysis, the urokinase receptor. We report that epithelial cells expressing full-length *vÎ²6 exhibit decreased urokinase receptor expression and function. Furthermore, this novel modulation requires the C-terminal 11 amino acids of the cytoplasmic tail of the Î²6 integrin subunit. Cells expressing *vÎ²3, however, did not affect urokinase receptor expression. De novo expression of Î²6 by melanoma cells and Î²3 by epithelial cells did not influence urokinase receptor expression or function, suggesting that modulation of urokinase system is both integrin subunit and cell-specific.
|Number of pages
|Biochemical and Biophysical Research Communications
|Published - 2004