MicroRNA-29a promotes the proliferation of human nasal epithelial cells and inhibits their apoptosis and promotes the development of allergic rhinitis by down-regulating FOS expression

PLoS One. 2021 Aug 12;16(8):e0255480. doi: 10.1371/journal.pone.0255480. eCollection 2021.

Abstract

Objective: To explore the regulation of microRNA-29a (miR-29a) on FOS in human nasal epithelial cells and its molecular mechanism, as well as the effects of miR-29a on the cell proliferation and apoptosis.

Methods: By cell transfection, gene silencing, quantitative real-time polymerase chain reaction (qRT-PCR), flow cytometry and TUNEL assay (for cell apoptosis), CCK-8 assay (for cell proliferation), dual-luciferase reporter gene assay and Western Blot, it was validated that miR-29a promoted the proliferation of human nasal epithelial cells and inhibited their apoptosis by down-regulating FOS expression in RPMI2650 and HNEpC cell lines.

Results: ①Compared with healthy controls, miR-29a expression was up-regulated and FOS mRNA expression was down-regulated in the nasal tissues from the patients with allergic rhinitis (AR). ②MiR-29a over-expression promoted the proliferation of RPMI2650 cells and HNEpC cells but inhibited their apoptosis. ③MiR-29a targeted at FOS. ④MiR-29a over-expression and FOS silencing both significantly promoted cell proliferation and inhibited cell apoptosis. After transfection with both miR-29a and FOS, there was a decrease in the proliferation but an increase in the apoptosis of cells.⑤MiR-29a promoted the proliferation of human nasal epithelial cells and inhibited their apoptosis by down-regulating FOS expression.

Conclusion: MiR-29a-/FOS axis can be regarded as a potential marker and a new therapy for AR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Case-Control Studies
  • Cell Proliferation
  • Cells, Cultured
  • Epithelial Cells / metabolism
  • Epithelial Cells / pathology*
  • Gene Expression Regulation*
  • Humans
  • MicroRNAs / genetics*
  • Nasal Mucosa / metabolism
  • Nasal Mucosa / pathology*
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism*
  • Rhinitis, Allergic / genetics
  • Rhinitis, Allergic / metabolism
  • Rhinitis, Allergic / pathology*

Substances

  • FOS protein, human
  • MIRN29a microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-fos

Grants and funding

This study was supported by the National Natural Science Foundation of China (82060497) and the Shenzhen Key Medical Discipline Construction Fund (SZXK039). The funders include Pro. Juan-Feng and Xianhai-Zeng. In addition, Pro.Yiqing-Zheng also helped with the review & editing of the paper.