Background: Considerable data have shown that circular RNAs (circRNAs) mediate the pathogenesis of chronic obstructive pulmonary disease (COPD). The study aims to analyze the function and mechanism of circ_0026466 in COPD. Methods: Human bronchial epithelial cells (16HBE) were treated with cigarette smoke extract (CSE) to establish a COPD cell model. Quantitative real-time polymerase chain reaction and Western blot were used to detect the expression of circ_0026466, microRNA-153-3p (miR-153-3p), TNF receptor associated factor 6 (TRAF6), cell apoptosis-related proteins, and NF-κB pathway-related proteins. Cell viability, proliferation, apoptosis, and inflammation were investigated by cell counting kit-8, EdU assay, flow cytometry, and enzyme-linked immunosorbent assay, respectively. Oxidative stress was evaluated by lipid peroxidation malondialdehyde assay kit and superoxide dismutase activity assay kit. The interaction between miR-153-3p and circ_0026466 or TRAF6 was confirmed by dual-luciferase reporter assay and RNA pull-down assay. Results: Circ_0026466 and TRAF6 expression were significantly increased, but miR-153-3p was decreased in the blood samples of smokers with COPD and CSE-induced 16HBE cells when compared with controls. CSE treatment inhibited the viability and proliferation of 16HBE cells but induced cell apoptosis, inflammation, and oxidative stress, but these effects were attenuated after circ_0026466 knockdown. Circ_0026466 interacted with miR-153-3p and regulated CSE-caused 16HBE cell damage by targeting miR-153-3p. Additionally, TRAF6, a target gene of miR-153-3p, regulated CSE-induced 16HBE cell injury by combining with miR-153-3p. Importantly, circ_0026466 activated NF-κB pathway by targeting the miR-153-3p/TRAF6 axis. Conclusion: Circ_0026466 absence protected against CSE-triggered 16HBE cell injury by activating the miR-153-3p/TRAF6/NF-κB pathway, providing a potential therapeutic target for COPD.
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