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Background <p>Pulmonary 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.</p> Methods <p>This 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.</p> Results <p>In 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.</p> Conclusion <p>LUCAT1 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.</p>

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Therapeutic potential of the LUCAT1/miR- 2278/STAT5A axis in pulmonary fibrosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月14日

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  • Juan Huang,
  • Weiqiang Zhang

摘要

Background

Pulmonary 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.

Methods

This 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.

Results

In 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.

Conclusion

LUCAT1 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.