{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T06:10:44Z","timestamp":1772950244910,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T00:00:00Z","timestamp":1623628800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Laboratory Analysis"],"published-print":{"date-parts":[[2021,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Chronic obstructive pulmonary disease (COPD), characterized by persistent airflow limitation, was a disease mediated by a combination of inflammatory factors, immune cells, and immune mediators. COPD was an inflammatory and autoimmune disease involving T\u2010lymphocytes triggered by cigarette smoke and other factors that progressively affected the bronchi, lung parenchyma, and pulmonary blood vessels. LncRNAs were reported to be implicated in COPD pathogenesis and development.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Non\u2010smokers, smokers (non\u2010COPD), and COPD patients were randomly selected in an established COPD surveillance cohort. Demographic and clinical information of all subjects were collected. Pulmonary function was measured by post\u2010bronchodilator testing. qRT\u2010PCR and ELISA assays were performed to detect the expression levels of lncRNA LUCAT1, miR\u2010181a\u20105p, and inflammatory cytokines. An in vitro exposure model was constructed using cigarette smoke extract (CSE)\u2010induced human bronchial epithelial (16HBE) cells. The dual\u2010luciferase reporter and RNA pull\u2010down assays were used to detect the binding relationship between lncRNA LUCAT1 and miR\u2010181a\u20105p; meanwhile, Spearman's correlation assay was used to verify the correlation between lncRNA LUCAT1 and miR\u2010181a\u20105p. Afterward, the lncRNA LUCAT1 silencing plasmid was constructed and co\u2010transfected with a miR\u2010181a\u20105p inhibitor to evaluate the effects on CSE\u2010induced 16HBE cell proliferation and apoptosis. Finally, a Western blot assay was utilized to determine the mechanism of lncRNA LUCAT1\/miR\u2010181a\u20105p\/Wnt\/\u03b2\u2010catenin axis in COPD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>LncRNA LUCAT1 was upregulated in the serums of COPD patients. Correlation analysis further confirmed the strong correlation between LUCAT1 expression and inflammatory cytokines IL\u20101\u03b2, IL\u20106, and TNF\u2010\u03b1. Receiver operating characteristic (ROC) analysis verified the potential of LUCAT1 in COPD diagnosis. After treatment with CSE, LUCAT1 was significantly increased while its target miR\u2010181a\u20105p was decreased in 16HBE cells. Cell proliferation and apoptosis assays showed that LUCAT1 silencing alleviated CSE\u2019s effects on 16HBE cell proliferation and apoptosis. Mechanically, rescue assays demonstrated that miR\u2010181a\u20105p inhibition could partially counteract the impact of LUCAT1 on COPD progression through the Wnt\/\u03b2\u2010catenin pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>LncRNA LUCAT1 may be a valuable indicator for differentiating COPD. Moreover, LncRNA LUCAT1\/miR\u2010181\u20105p\/Wnt\/\u03b2\u2010catenin axis behaved as a critical role in COPD development, shedding new sights for clinical treatment.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcla.23823","type":"journal-article","created":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T18:10:31Z","timestamp":1623694231000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Expression of long non\u2010coding RNA LUCAT1 in patients with chronic obstructive pulmonary disease and its potential functions in regulating cigarette smoke extract\u2010induced 16HBE cell proliferation and apoptosis"],"prefix":"10.1002","volume":"35","author":[{"given":"Shan","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory Affiliated Yixing People\u2019s Hospital Jiangsu University  Wuxi 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