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Urokinase-type plasminogen activator receptor (uPAR) expression enhances invasion and metastasis in RAS mutated tumors. 2017
Concetta Di Mauro, and
Ada Pesapane, and
Luigi Formisano, and
Roberta Rosa, and
Valentina D'Amato, and
Paola Ciciola, and
Alberto Servetto, and
Roberta Marciano, and
Roberta Clara Orsini, and
Francesca Monteleone, and
Nicola Zambrano, and
Gabriella Fontanini, and
Adele Servadio, and
Giuseppe Pignataro, and
Lucia Grumetto, and
Antonio Lavecchia, and
Dario Bruzzese, and
Antonino Iaccarino, and
Giancarlo Troncone, and
Bianca Maria Veneziani, and
Nunzia Montuori, and
Sabino De Placido, and
Roberto Bianco
Department of Clinical Medicine and Surgery, University of Naples "Federico II", Naples, Italy.
The urokinase-type plasminogen activator receptor (uPAR) is a GPI-anchored cell membrane receptor that focuses urokinase (uPA) proteolytic activity on the cell surface. Its expression is increased in many human cancers, including non-small cell lung cancer (NSCLC) and colorectal cancer (CRC), and correlates with a poor prognosis and early invasion and metastasis. uPAR is able to control, through a cross-talk with tyrosine kinase receptors, the shift between tumor dormancy and proliferation, that usually precedes metastasis formation. Therefore, we investigated the role of uPAR expression in RAS mutated NSCLC and CRC cells. In this study we provided evidence, for the first time, that RAS mutational condition is functionally correlated to uPAR overexpression in NSCLC and CRC cancer cell lines and patient-derived tissue samples. Moreover, oncogenic features related to uPAR overexpression in RAS mutated NSCLC and CRC, such as adhesion, migration and metastatic process may be targeted, in vitro and in vivo, by new anti-uPAR small molecules, specific inhibitors of uPAR-vitronectin interaction. Therefore, anti-uPAR drugs could represent an effective pharmacological strategy for NSCLC and CRC patients carrying RAS mutations.
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