Abstract
Met is a tyrosine kinase receptor, encoded by an oncogene, whose crucial role has been elucidated during the last two decades. The complex biological program triggered by Met has been dissected and its biological relevance in both physiology and pathology has been proven. Met supports a morphogenetic program, known as invasive growth, taking place both during embryogenesis and adulthood. In tumors Met is often aberrantly activated, giving rise to the pathological counterpart of the invasive growth program: cancer progression towards metastasis. Several approaches have been recently developed to interfere with the tumorigenic and metastatic processes triggered by Met.
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Acknowledgements
We would like to thank Andrea Bertotti for micrographs. Work in the authors’ laboratory is supported by AIRC (Associazione Italiana per la Ricerca sul Cancro), MIUR (Ministero dell’Isruzione, Universita’ e Ricerca), Compagnia San Paolo, Fondazione Cassa di Risparmio di Torino. AG is supported by an AIRC fellowship.
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During the revision of this review, another paper was published that demonstrated reduced proliferation, xenograft growth and experimental metastasis formation following shRNA-mediated down-regulation of MET in a gastric carcinoma cell line with amplification of MET gene [86].
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Gentile, A., Trusolino, L. & Comoglio, P.M. The Met tyrosine kinase receptor in development and cancer. Cancer Metastasis Rev 27, 85–94 (2008). https://doi.org/10.1007/s10555-007-9107-6
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DOI: https://doi.org/10.1007/s10555-007-9107-6