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Research Paper

Exosomal miR-211 derived from cancer stem cells promotes cancer progression by activating autophagy in NSCLC

Xiaoxue Zhang1, Yan Chen2, Yongchao Yu3, Shu Zhu1, Jing Zhang1, Yan Wang1, Xiangyun Zhang1
  • 1Department of Oncology, Hiser Medical Center of Qingdao, Qingdao 266001, Shandong Province, China
  • 2Department of Urologic Surgery, Hiser Medical Center of Qingdao, Qingdao 266001, Shandong Province, China
  • 3Department of Intervention, Hiser Medical Center of Qingdao, Qingdao 266001, Shandong Province, China
Received: March 28, 2020Accepted: June 29, 2020
https://doi.org/10.18632/aging.103680

Copyright: © 2021 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.