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CircZNF609 regulates pulmonary fibrosis via miR-145-5p/KLF4 axis and its translation function

Wenqing Sun1, Siyun Zhou1, Lan Peng1

  • 1Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.

Cellular & Molecular Biology Letters
|December 17, 2023
PubMed
Abstract

Insights

Circular RNA ZNF609 (circZNF609) is downregulated in silica-induced pulmonary fibrosis. Upregulating circZNF609 inhibits fibroblast activation and lung fibrosis, offering a potential new therapeutic target.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Pulmonary Medicine

Background:

  • Pulmonary fibrosis is a progressive lung disease with limited treatment options.
  • The pathogenesis of silica-induced pulmonary fibrosis is not fully understood.
  • Circular RNAs (circRNAs) are implicated in disease but their role in silica-induced pulmonary fibrosis is unclear.

Purpose of the Study:

  • To investigate the role of circZNF609 in silica-induced pulmonary fibrosis.
  • To elucidate the molecular mechanism of circZNF609 in fibroblast activation.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) to measure gene expression.
  • RNA immunoprecipitation (RIP) and m6A RNA immunoprecipitation (MeRIP) assays.
  • In vitro studies with fibroblast cell lines and in vivo studies with silica-induced mouse models.

Main Results:

  • circZNF609 was downregulated in activated fibroblasts and fibrotic lung tissues.
  • Overexpression of circZNF609 inhibited fibroblast activation and silica-induced lung fibrosis in mice.
  • circZNF609 regulates pulmonary fibrosis via the miR-145-5p/KLF4 axis and circZNF609-encoded peptides, with its expression modulated by N6-methyladenosine (m6A) modification.

Conclusions:

  • circZNF609 is a critical regulator of fibroblast activation and silica-induced pulmonary fibrosis.
  • circZNF609 and its derived peptides show promise as novel therapeutic targets for pulmonary fibrosis.
Keywords:
Coding capacityNon-coding RNASilicosiscircZNF609

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