Exosomal miR-181a-3p Regulates the Anlotinib Resistance of Lung Cancer Cells

Abstract

This study investigates the mechanism of Anlotinib in the treatment of lung cancer drug resistance. A total of 30 lung cancer tissue specimens were retrospectively analyzed and 30 normal lung tissues were included as a control. Real-time PCR detected miR-181a-3p expression along with analysis of cell viability by MTT assay, cell invasion by transwell, and the exosomal miR-181a-3p/UPR/ERAD signaling pathway. The expression of miR-181a-3p in peripheral blood of lung cancer was increased and the overall survival rate of patients with high miR-181a-3p in exosomes was shorter than patients with low expression. In A549 and H292 cell lines, anlotinib is added to overexpress exosomal miR-181a-3p, cell viability and invasion were significantly increased. After knocking down exosomal miR-181a-3p, cell viability and invasion were significantly reduced. The expression of miR-181a-3p is directly regulated by exosomes UPR/ERAD. After overexpression of exosomes miR-181a-3p, the protein levels of UPR and ERAD were significantly reduced and increased after knockdown of exosomes miR-181a-3p. In conclusion, the secretory miR-181a-3p/UPR/ERAD pathway promotes the proliferation of A549 and H292 cells, regulates the resistance of Anlotinib, and can increase the resistance of lung cancer to Anlotinib by promoting the proliferation signaling pathway, and promote the growth of tumor cells.