ArticleBMC pulmonary medicine2025
Therapeutic potential of the LUCAT1/miR- 2278/STAT5A axis in pulmonary fibrosis.
Article in BMC pulmonary medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPulmonary fibrosis is a debilitating, progressive lung disorder marked by insidious onset and relentless decline. Emerging evidence highlights the regulatory significance of long non-coding RNAs (lncRNAs) in fibrotic processes.
methodsThis study investigated the mechanistic role of lncRNA LUCAT1 in pulmonary fibrosis using TGF-β-stimulated A549 cells as an in vitro model. The methodologies employed include qPCR and Western blot to assess gene and protein expression, CCK-8 assays to evaluate cell viability, cell migration assays for assessing mobility, and dual-luciferase reporter assays to analyze miRNA interactions.
resultsIn A549 cells treated with TGF-β, LUCAT1 expression increased. After LUCAT1 was silenced, both cell vitality and exercise ability promoted by TGF-β were reduced. Inhibition of LUCAT1 increases E-cadherin levels and decreases the expression of α-SMA and Collagen I. LUCAT1 interacts with miR-2278. Blocking miR-2278 prevented the reduction in proliferation, migration, and epithelial-to-mesenchymal transformation (EMT) in TGF-β-treated A549 cells due to knock-out of LUCAT1. Similarly, inhibition of miR-2278 also eliminated the decline in proliferation, migration, and EMT in TGF-β stimulated A549 cells due to inhibition of LUCAT1.
conclusionLUCAT1 knockdown targeted STAT5A by sponging miR-2278 to inhibit the TGF-β-induced proliferation, migration, and EMT in A549 cells, stretching the treatment strategy of lung epithelial injury.
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