Epidermal growth factor receptor (EGFR) T790 M mutation act as the dominant resistance mechanism to first and second generations tyrosine kinase inhibitors (TKIs), the roles of miR-7 in the development of T790 M mutation are largely unknown. Here, we confirmed that the level of miR-7 was significantly higher in the gefitinib sensitivity PC9 cells compared to gefitinib resistance H1975 cells, and miR-7 overexpression promoted the apoptosis of H1975 cells by gefitinib treatment. Furthermore, we found that exosomes could transfer miR-7 mimics from PC9 cells to H1975 cells, which reversed gefitinib resistance through binding to YAP, and altered H1975 cells resistance phenotype in vitro. In addition, we suppressed exosomal miR-7 by GW4869, increasing PC9 cells chemoresistance to gefitinib treatment in vivo. Of note, we detected that miR-7 was significantly higher in serum exosomes from healthy controls than from patients with lung carcinoma, and high miR-7 expression was associated with strong response to lung carcinoma patients receiving gefitinib treatment, as well as a longer survival. Therefore, exosomal miR-7 can act as a potential biomarker and therapeutic target for EGFR T790 M resistance mutations.
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