Long non-coding RNA NNT-AS1 regulates proliferation, apoptosis, inflammation and airway remodeling of chronic obstructive pulmonary disease via targeting miR-582-5p/FBXO11 axis

[Display omitted] •NNT-AS1 silence reversed CSE-induced proliferation, apoptosis, inflammation and airway remodeling in vitro.•MiR-582-5p could bind to NNT-AS1 in HBE cells.•FBXO11 is the target gene of miR-582-5p.•MiR-582-5p inhibitor reversed the biological effects of NNT-AS1 knockdown.•NNT-AS1 regulates COPD development via targeting miR-582-5p/FBXO11 axis. Chronic obstructive pulmonary disease (COPD) is a kind of chronic lung disease that mainly induced by smoking-caused inflammation. Long non-coding RNAs (lncRNAs) have been reported to play a part in the course of pulmonary diseases. Here, we studied the role of lncRNA NNT-AS1 in the development of COPD. qRT-PCR analysis and ELISA assay were applied to evaluate the expression of genes and inflammatory cytokines, respectively. CCK8 and EdU assays were utilized to assess proliferation, while flow cytometry assay was conducted to evaluate apoptosis. Luciferase reporter, RNA pull down and RIP assays were combined to explore relationships between genes. NNT-AS1 was observed to be up-regulated in cigarette smoke extract (CSE)-treated 16HBE cells. Knockdown of NNT-AS1 abolished CSE-caused suppressive effects on cell proliferation, apoptosis, inflammation and airway remodeling. Mechanistically, NNT-AS1 up-regulated FBXO11 expression via sponging miR-582-5p. Moreover, miR-582-5p inhibitor or FBXO11 overexpression counteracted NNT-AS1 silence-elicited effects on proliferation, apoptosis, inflammation and airway remodeling. Our data revealed that NNT-AS1 played a promoting role in smoking-induced COPD via modulating miR-582-5p/FBXO11 signaling, suggesting a novel potential target for COPD treatment.