miR-1-3p and miR-206 sensitizes HGF-induced gefitinib-resistant human lung cancer cells through inhibition of c-Met signalling and EMT.

摘要: Hepatocyte growth factor (HGF) overexpression is an important mechanism in acquired epidermal receptor (EGFR) kinase inhibitor gefitinib resistance lung cancers with EGFR activating mutations. MiR-1-3p and miR-206 act as suppressors cancer proliferation metastasis. However, whether miR-1-3p can overcome HGF-induced mutant not clear. In this study, we showed that restored the sensitivities of cells PC-9 HCC-827 to present HGF. For mechanisms, demonstrated both directly target HGF c-Met cancer. Knockdown mimicked effects transfections Meanwhile, attenuated cancers. Furthermore, inhibited downstream Akt Erk pathway blocked epithelial-mesenchymal transition (EMT). Finally, increase sensitivity xenograft mouse models vivo. Our study for first time indicated new function overcoming cell.