ArticleBMC pulmonary medicine2025
LncRNA IGF2-AS serves as a miR-106b-5p sponge to induce apoptosis and inflammatory reaction of bronchial epithelial cells in COPD.
Article in BMC pulmonary medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- FOXD2-AS1/miR-185-5p/CDC42 axis in chronic obstructive pulmonary disease: clinical significance and mechanistic insights.Journal of inflammation (London, England) · 2026Article
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7 authors.
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Abstract
backgroundThe incidence and fatality rates of chronic obstructive pulmonary disease (COPD) are increasing, and the acute exacerbation of COPD (AECOPD) causes poor prognosis in patients.
aimThis study evaluated the clinical role of serum lncRNA IGF2-AS in stable COPD and AECOPD and explored its functional mechanism in bronchial epithelial cells.
methodsBlood 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.
resultsThe 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.
conclusionLncRNA 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.
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