The knockdown of MEG3 could directly target miR-149-3p to inhibit the activation of the NF-κB signalling pathway and promote proliferation while inhibiting apoptosis of CSE-treated HBE cells, suggesting that MEG3/miR-149-3p/NF-κB axis has a crucial function in the pathogenesis of COPD. This evidence concerns the gene NFKB1 and chronic obstructive pulmonary disease.