MET and cancer: Upon HGF binding, c-Met dimerizes, transphosphorylates, and activates downstream signaling through several pathways with diverse cellular functions that are important in cancer progression, including the Ras-related C3 botulinum toxin substrate 1 (Rac1)/ cell division control protein 42 homolog (Cdc42) pathway, the phosphoinositide-3 kinase (PI3K)/protein kinase B (Akt) pathway, breast tumor kinase (Brk) and phospholipase C-γ pathways as well as the extracellular signal regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) cascade [2, 3, 8].