miR-141 regulation of EIF4E expression affects docetaxel chemoresistance of non-small cell lung cancer.

The present study investigated the role of miR-141 regulation of eukaryotic initiation factor-4E (EIF4E) expression in docetaxel chemoresistance of human non-small cell lung cancer (NSCLC). The expression of miR-141 in docetaxel chemoresistant patients with NSCLCs was markedly higher than those of non-docetaxel chemoresistant patients with NSCLCs. The expression of EIF4E in docetaxel chemoresistant patients with NSCLCs was markedly lower than those of non-docetaxel chemoresistant patients with NSCLCs. Downregulation of miR-141 suppressed cell proliferation, induced cell death and increased caspase-3 activity in H1299 or H2009/docetaxel cells. Downregulation of miR-141 also increased the protein expression of EIF4E, VEGF, c-Myc and Bax in H1299 or H2009/docetaxel cells. Conversely, up-regulation of miR-141 promoted cell proliferation, inhibited cell death and caspase-3 activity in H1299 or H2009/docetaxel cell. Upregulation of miR-141 suppressed EIF4E, VEGF, c-Myc protein expression and inhibited Bax in H1299 or H2009/docetaxel cells. Thus, the present study is the first to show the induction of miR-141/EIF4E expression in an acquired model of docetaxel chemoresistant patients with NSCLCs. This serves as a mechanism of acquired docetaxel chemoresistant patients with NSCLCs, possibly through direct interactions with VEGF, c-Myc, and Bax, therefore presenting a potential therapeutic target for the treatment of docetaxel chemoresistant patients with NSCLCs.