Knockdown of circ_0006872 alleviates CSE-induced human bronchial epithelial cells injury in chronic obstructive pulmonary disease.

Circular RNAs (circRNAs) have been reported to be related to the initiation and progression of chronic obstructive pulmonary disease (COPD) by affecting the function of human bronchial epithelial cells (HBECs). Here, we aimed to investigate the function and mechanism of circ_0006872 in regulating COPD process using cigarette smoke extract (CSE)-induced 16HBEC in vitro. The results showed that circ_0006872 was increased in smokers without or with COPD, especially in smokers with COPD. Also, its expression was dose-dependently up-regulated by CSE exposure in 16HBECs. Functionally, circ_0006872 knockdown dramatically attenuated CSE-evoked proliferation arrest, apoptosis, inflammatory response and oxidative stress in 16HBECs. Mechanistically, circ_0006872/miR-485-3p/cyclin-dependent kinase inhibitor 1B (CDKN1B) formed a competitive endogenous RNA (ceRNA) network. CDKN1B was increased and miR-485-3p was decreased in COPD patients and CSE-induced 16HBECs. MiR-485-3p overexpression or CDKN1B knockdown protected 16HBEC against CSE-induced 16HBEC injury mentioned above. Moreover, rescue experiments showed that circ_0006872 regulated CSE-induced 16HBEC injury via miR-485-3p/CDKN1B axis. Circ_0006872 silencing protected against CSE-induced bronchial epithelial cell injury via miR-485-3p/CDKN1B axis, suggesting the potential application of circ_0006872 in preventing cigarette smoke-induced COPD. [ABSTRACT FROM AUTHOR]