Authors
Jinong Zhao, Yan Zhang, Lijuan Gao, Yiping Tang
Published in
COPD. Volume 23. Issue 1. Pages 2658219. Epub Jun 22, 2026.
Abstract
Long non-coding RNA MIR31HG (lncRNA MIR31HG) plays a well-defined role in tumor progression. However, its roles in chronic obstructive pulmonary disease (COPD) progression remain elusive. This study aimed to investigate the expression level and the physiological role of lncRNA MIR31HG in COPD, and further examine the relationship of the lncRNA MIR31HG and miR-342-3p with disease severity, clinical features, and inflammation levels.
Serum levels of lncRNA MIR31HG and miR-342-3p were measured by RT‑qPCR in healthy controls (HC), patients with stable COPD, and those with acute exacerbation COPD (AECOPD). An in vitro model simulating COPD was created through treatment of Beas-2B cells with 2% cigarette smoke extract (CSE). Cell proliferation and inflammatory cytokines were detected by CCK-8 method and ELISA respectively. The relationship between lncRNA MIR31HG and miR-342-3p was examined using dual luciferase reporter and rescue assays.
The expression of lncRNA MIR31HG was up-regulated in COPD patients and CSE-exposed Beas-2B cells. LncRNA MIR31HG positively regulated COPD-related malignant characteristics. The silencing of lncRNA MIR31HG alleviated the slow cell proliferation and inflammation caused by CSE exposure. The expression level of miR-342-3p was more attenuated in COPD patients compared with HC. Assays confirmed that lncRNA MIR31HG participates in cell proliferation and inflammatory response by targeting miR-342-3p.
The lncRNA MIR31HG expression was increased in patients with COPD. Its level was positively correlated with disease severity and inflammation but negatively associated with miR-342-3p. LncRNA MIR31HG might be an effective target for COPD distinction and treatment.
PMID:
42328967
Bibliographic data and abstract were imported from PubMed on 22 Jun 2026.
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