Fig. 1

HGF/SF-mediated activation of c-Met and relayed downstream signalling. The c-Met receptor can be structured into distinct domains, including sema, cysteine-rich, immunoglobulin, trans-membrane, juxta-membrane, tyrosine kinase, and C-terminal region. Pharmacological intervention with activated c-Met signalling includes: (i) competitive interference with HGF/c-Met interaction, (ii) inhibition of the tyrosine kinase activity of c-Met with the use of tyrosine kinase inhibitors (TKI), or (iii) blocking of activated c-Met downstream signaling mediators. Accordingly, cell fate and development such as survival, transformation, cell motility, and proliferative capacity can be affected. This figure was adapted from Organ and Tsao, 2011 [2]