LncRNA IGF2-AS serves as a miR-106b-5p sponge to induce apoptosis and inflammatory reaction of bronchial epithelial cells in COPD.

Abstract

Background: The incidence and fatality rates of chronic obstructive pulmonary disease (COPD) are increasing, and the acute exacerbation of COPD (AECOPD) causes poor prognosis in patients.

Aim: This study evaluated the clinical role of serum lncRNA IGF2-AS in stable COPD and AECOPD and explored its functional mechanism in bronchial epithelial cells.

Methods: Blood samples were obtained from COPD patients and controls. The RT-qPCR analysis was performed to detect the expression of IGF2-AS in serum samples and cells. Cell proliferation, cell apoptosis, and inflammation response were detected by CCK-8 assay, flow cytometry assay, and ELISA assay. Targeted regulation of IGF2-AS and miR-106b-5p was confirmed by dual-luciferase reporter assay.

Results: The serum IGF2-AS was increased in stable COPD patients and AECOPD patients compared to healthy controls. Increased IGF2-AS expression had diagnostic value in distinguishing COPD patients from healthy control and differentiating AECOPD patients from stable COPD patients. Silencing IGF2-AS abolished the effects of 2% cigarette smoke extract (CSE) on 16HBE cell behaviors and inflammatory factors (IL-1β, IL-6, TNF-α). miR-106b-5p partially reversed the influence of IGF2-AS on CSE-treated 16HBE cell proliferation, apoptosis, and inflammatory response.

Conclusion: LncRNA IGF2-AS which is upregulated in patients with COPD (especially AECOPD) might be a potential diagnostic biomarker for ADCOPD. Low expression of IGF2-AS can promote the proliferation ability, and reduce apoptosis, and inflammation response of CSE-treated 16HBE cells by targeting miR-106b-5p.