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

Grant support

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.