In CEM cells the autosomal deafness gene dfna5 is regulated by glucocorticoids and forskolin

J Steroid Biochem Mol Biol. 2007 Oct;107(1-2):15-21. doi: 10.1016/j.jsbmb.2007.02.004. Epub 2007 May 24.

Abstract

Certain mutations of the dfna5 gene result in a form of autosomal deafness that holds special interest because its phenotype resembles the hearing loss often seen during aging. Little is known of the function or regulation of dfna5 or its encoded protein. However dfna5 has recently been shown to be induced by p53. It also is epigenetically repressed in gastric cancer. We have discovered that dfna5 can be induced by glucocorticoids (GCs) and that this regulation is influenced by crosstalk with the protein kinase A (PKA) system. We show that GCs induce dfna5 mRNA and that its expression appears to be repressed in the basal state. Induction of dfna5 mRNA correlates with GC-dependent apoptosis of CEM cells, though dfna5 expression alone is not sufficient for apoptosis.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Apoptosis
  • Cell Line, Tumor
  • Colforsin / pharmacology*
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Dexamethasone / pharmacology*
  • Gene Expression Regulation
  • Glucocorticoids / pharmacology*
  • Humans
  • Mutation
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Receptors, Estrogen / biosynthesis*
  • Receptors, Estrogen / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • GSDME protein, human
  • Glucocorticoids
  • RNA, Messenger
  • Receptors, Estrogen
  • Tumor Suppressor Protein p53
  • Colforsin
  • Dexamethasone
  • Cyclic AMP-Dependent Protein Kinases