Relationship between abnormal activation of HGF/c-Met signaling pathway and EGFR-TKI acquired resistance in non-small cell lung cancer

Targeted therapy such as the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) has made huge progress in treatment of non-small cell lung cancer (NSCLC). However, the emergence of acquired drug resistance is an inevitable result of the targeted therapy. The hepatocyte growth factor/c-mesenchymal-epithelial transition factor (HGF/c-Met) signaling pathway participates in cell formation, migration, angiogenesis and other important cellular processes of multiple tumors. The abnormal activation of this signaling pathway plays the pivotal role in the acquired resistance to EGFR-TKI. Recently, some clinic trials prove that HGF/c-Met inhibitors can make clinical benefit of some NSCLC patients with acquired drug resistance of EGFR-TKI. Key words: Proto-oncogene protein c-met; Hepatocyte growth factor; Carcinoma, non-small-cell lung