Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell lines

摘要

PurposeAcquired resistance to erlotinib in patients with EGFR-mutant non-small cell lung cancer can result from aberrant activation of alternative receptor tyrosine kinases, such as the HGF-driven c-MET receptor. We sought to determine whether inhibition of AKT signaling could augment erlotinib activity and abrogate HGF-mediated resistance.