m6A RNA methylation regulators could contribute to the occurrence of chronic obstructive pulmonary disease

J Cell Mol Med. 2020 Nov;24(21):12706-12715. doi: 10.1111/jcmm.15848. Epub 2020 Sep 22.

Abstract

N6-methyladenosine (m6A) RNA methylation, the most prevalent internal chemical modification of mRNA, has been reported to participate in the progression of various tumours via the dynamic regulation of m6A RNA methylation regulators. However, the role of m6A RNA methylation regulators in chronic obstructive pulmonary disease (COPD) has never been reported. This study aimed to determine the expression and potential functions of m6A RNA methylation regulators in COPD. Four gene expression data sets were acquired from Gene Expression Omnibus. Gene ontology function, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses, weighted correlation network analysis and protein-protein interaction network analysis were performed. The correlation analyses of m6A RNA methylation regulators and key COPD genes were also performed. We found that the mRNA expressions of IGF2BP3, FTO, METTL3 and YTHDC2, which have the significant associations with some key genes enriched in the signalling pathway and biological processes that promote the development progression of COPD, are highly correlated with the occurrence of COPD. In conclusion, six central m6A RNA methylation regulators could contribute to the occurrence of COPD. This study provides important evidence for further examination of the role of m6A RNA methylation in COPD.

Keywords: IGF2BP3; METTL3; bioinformatics; chronic obstructive pulmonary disease; m6A RNA methylation regulators.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine / analogs & derivatives*
  • Adenosine / metabolism
  • Case-Control Studies
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Gene Ontology
  • Humans
  • Methylation
  • Pulmonary Disease, Chronic Obstructive / genetics*
  • RNA / metabolism*

Substances

  • RNA
  • N-methyladenosine
  • Adenosine