c-Met is a receptor tyrosine kinase (RTK) with hepatocyte growth factor (HGF) as its natural ligand. c-Met may be activated in a ligand-dependent manner by binding HGF or in a ligand-independent manner. Diverse activation mechanisms of c-Met exist in many malignant tumors, including lung cancer. Moreover, the abnormal activation of c-Met has a close relationship with the occurrence, development and malignant biological behavior of lung cancer. This paper focused on the different activation mechanisms of c-Met in non-small cell lung cancer and small cell lung cancer and also reviewed the research progress of c-Met targeted drugs in lung cancer.