Abstract

Background: Non-small cell lung cancer (NSCLC) has the highest clinical incidence in all of types lung cancer, which seriously affects people’s lives and increases the financial burden of medical care. Therefore, it is crucial to identify the molecular mechanisms and pathways of lung cancer occurrence and development, and find more effective treatment methods and targeted drugs.

Results: MiR-211 was highly expressed in CSC exosomes, and exosomal miR-211 mainly derived from CSCs in NSCLC. CSCs exosomes co-cultured with NSCLC cells promoted the viability, migration and invasion of NSCLC cells. Furthermore, exo-miR-211 promoted NSCLC cells autophagy, and inhibition of autophagy with autophagy inhibitor 3-MA reversed CSC-derived exo-miR211 promoting effects on NSCLC progression. Further analysis showed BCL-W was a direct target of miR-211, and miR-211 facilitated cancer progression and autophagy in NSCLC cells via BCL-W inhibition. In vivo tumorigenesis assay showed CSC-derived exo-miR-211 enhanced NSCLC progression and promoted autophagy.

Conclusion: Our study suggested CSCs derived exo-miR-211 promoted NSCLC progression by activating autophagy via targeting BCL-W, which might provide a new idea for NSCLC treatment.