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MiR-203a-3p regulates TGF-β1-induced epithelial-mesenchymal transition (EMT) in asthma by regulating Smad3 pathway

Qi Fan1, Yu Jian1

  • 1Department of Emergency Medicine, Jingzhou Central Hospital, Jingzhou, Hubei, China.

Bioscience Reports
|February 18, 2020
PubMed

Insights

MicroRNA miR-203a-3p, down-regulated in asthma, inhibits airway epithelial-mesenchymal transition by targeting SIX1. This mechanism involves the Smad3 pathway, offering potential therapeutic insights for asthma treatment.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Respiratory Medicine

Background:

  • Asthma is a prevalent chronic airway disease with increasing incidence.
  • MicroRNAs (miRNAs) are key regulators of cellular processes, including those implicated in asthma pathogenesis.
  • Understanding the specific roles of miRNAs in asthma is crucial for developing targeted therapies.

Purpose of the Study:

  • To elucidate the molecular mechanism of miR-203a-3p in asthma development.
  • To investigate the regulatory relationship between miR-203a-3p and Sine oculis homeobox homolog 1 (SIX1).
  • To determine the role of the miR-203a-3p/SIX1 axis in transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT).

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) for gene expression analysis.
  • Western blot to assess protein levels of key molecules.
  • Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm miRNA-target interaction.
  • In vitro cell culture models (BEAS-2B and 16HBE cells) with TGF-β1 stimulation.

Main Results:

  • MiR-203a-3p was downregulated, while SIX1 was upregulated in asthma patient serums.
  • TGF-β1 treatment decreased miR-203a-3p and increased SIX1 expression in bronchial epithelial cells.
  • MiR-203a-3p directly targeted and negatively regulated SIX1.
  • Overexpression of miR-203a-3p or deletion of SIX1 reversed TGF-β1-induced EMT.
  • The miR-203a-3p/SIX1 axis regulated TGF-β1-mediated EMT via the Smad3 signaling pathway.

Conclusions:

  • MiR-203a-3p plays a protective role in asthma by inhibiting TGF-β1-induced EMT.
  • The miR-203a-3p/SIX1 interaction is a critical regulator of EMT in bronchial epithelial cells.
  • Targeting the miR-203a-3p/SIX1/Smad3 pathway presents a potential therapeutic strategy for asthma.
Keywords:
EMTSIX1Smad3TGF-β1asthmamiR-203a-3p

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