Non-small cell lung cancer (NSCLC) represents a highly prevalent and lethal malignant tumor on a global scale, with a substantial proportion of patients presenting with EGFR mutation-positive non-squamous NSCLC. While the use of EGFR tyrosine kinase inhibitors (EGFR-TKIs) targeted drugs has significantly enhanced the prognosis for these patients, the issue of drug resistance has progressively emerged as a critical concern, severely constraining their therapeutic efficacy. As a key signal transduction molecule, abnormal activation of Mesenchymal-epithelial transition factor (MET) protein has been proved to be one of the important reasons leading to EGFR-TKIs resistance in EGFR mutation-positive NSCLC patients. This article conducts a systematic review on the structure and physiological functions of the MET protein, thoroughly analyzing the molecular mechanism by which abnormal activation of the MET protein regulates the resistance to targeted therapy for EGFR-mutated NSCLC. It comprehensively summarizes the current intervention strategies and research progress for the resistance mediated by the MET protein, and looks forward to future research directions. The aim is to provide a theoretical basis and innovative research ideas for the precise treatment of patients with EGFR-mutated NSCLC.
Chen et al. (Sun,) studied this question.