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Research Paper|Volume 13, Issue 5|pp 7660—7675

Long noncoding RNA NR2F1-AS1 promotes the malignancy of non-small cell lung cancer via sponging microRNA-493-5p and thereby increasing ITGB1 expression

Chan Zhang1,2, Shangjie Wu1, Rong Song3, Changming Liu4
  • 1Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha 410000, Hunan, China
  • 2Department of Respiratory Medicine, The Fourth Hospital of Changsha, Changsha 410006, Hunan, China
  • 3Department of Anesthesiology, The Second Xiangya Hospital of Central South University, Changsha 410000, Hunan, China
  • 4Department of Infectious Diseases, The First Hospital of Changsha, Changsha 410000, Hunan, China
Received: April 3, 2020Accepted: June 5, 2020Published: August 7, 2020
https://doi.org/10.18632/aging.103564

Copyright: © 2020 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

Several studies have reported that the long noncoding ribonucleic acid (lncRNA) NR2F1 antisense RNA 1 (NR2F1-AS1) affects multiple cellular pathways that are involved in tumorigenesis and tumor progression. The present study aimed to detect NR2F1-AS1 expression in non-small cell lung cancer (NSCLC), investigate the role of NR2F1-AS1 in promoting the tumorigenic behavior of NSCLC cells, and elucidate the mechanism underlying the effect of NR2F1-AS1 on NSCLC progression. Our results showed that NR2F1-AS1 expression was upregulated in NSCLC cells, and notably, its upregulation was correlated with adverse clinical characteristics and shorter overall survival in patients with NSCLC. The absence of NR2F1-AS1 functionally decreased NSCLC cell proliferation, migration, and invasion and promoted tumor cell apoptosis. In addition, the tumor growth of NSCLC cells in vivo was inhibited after NR2F1-AS1 silencing. Mechanistically, NR2F1-AS1 functioned as a competing endogenous RNA for miR-493-5p and consequently increased ITGB1 expression. Rescue assays further validated that an increased output of the miR-493-5p/ITGB1 axis could neutralize the regulatory impact of NR2F1-AS1 knockdown on the malignant phenotype of NSCLC cells. In summary, the NR2F1-AS1/miR-493-5p/ITGB1 pathway initiates pro-oncogenic behavior in NSCLC tumor progression, and the NR2F1-AS1/miR-493-5p/ITGB1 axis may provide new molecular targets for anticancer therapy against NSCLC.