Cell-specific expression of ENACα gene by FOXA1 in the glucocorticoid receptor pathway

Int J Immunopathol Pharmacol. 2020 Jan-Dec:34:2058738420946192. doi: 10.1177/2058738420946192.

Abstract

Introduction: The glucocorticoid receptor (GR) is one of the most widely studied ligand-dependent nuclear receptors. The combination of transcriptional regulatory factors required for the expression of individual genes targeted by GR varies across cell types; however, the mechanisms underlying this cell type-specific regulation of gene expression are not yet clear.

Methods: Here, we investigated genes regulated by GR in two different cell lines, A549 and ARPE-19, and examined how gene expression varied according to the effect of pioneer factors using RNA-seq and RT-qPCR.

Results: Our RNA-seq results identified 19 and 63 genes regulated by GR that are ARPE-19-specific and A549-specific, respectively, suggesting that GR induces the expression of different sets of genes in a cell type-specific manner. RT-qPCR confirmed that the epithelial sodium channel (ENACα) gene is an ARPE-19 cell-specific GR target gene, whereas the FK506 binding protein 5 (FKBP5) gene was A549 cell-specific. There was a significant decrease in ENACα expression in FOXA1-deficient ARPE-19 cells, suggesting that FOXA1 might function as a pioneer factor enabling the selective expression of ENACα in ARPE-19 cells but not in A549 cells.

Conclusion: These findings indicate that ENACα expression in ARPE-19 cells is regulated by FOXA1 and provide insights into the molecular mechanisms of cell type-specific expression of GR-regulated genes.

Keywords: ENACα; FOXA1; glucocorticoid receptor; pioneer factor.

Publication types

  • Comparative Study

MeSH terms

  • A549 Cells
  • Dexamethasone / pharmacology
  • Epithelial Sodium Channels / genetics
  • Epithelial Sodium Channels / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Glucocorticoids / pharmacology
  • Hepatocyte Nuclear Factor 3-alpha / genetics
  • Hepatocyte Nuclear Factor 3-alpha / metabolism*
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • Receptors, Glucocorticoid / agonists
  • Receptors, Glucocorticoid / metabolism*
  • Retinal Pigment Epithelium / drug effects
  • Retinal Pigment Epithelium / metabolism*
  • Signal Transduction
  • Tacrolimus Binding Proteins / genetics
  • Tacrolimus Binding Proteins / metabolism*

Substances

  • Epithelial Sodium Channels
  • FOXA1 protein, human
  • Glucocorticoids
  • Hepatocyte Nuclear Factor 3-alpha
  • Receptors, Glucocorticoid
  • SCNN1A protein, human
  • Dexamethasone
  • Tacrolimus Binding Proteins
  • tacrolimus binding protein 5