p53-dependent transcriptional regulation of EDA2R and its involvement in chemotherapy-induced hair loss

FEBS Lett. 2010 Jun 3;584(11):2473-7. doi: 10.1016/j.febslet.2010.04.058. Epub 2010 Apr 29.

Abstract

The p53 tumor suppressor coordinates a multitude of cellular and organismal processes and exerts its activities mainly by activation of gene transcription. Here we describe the transcriptional activation of ectodysplasin A2 receptor (EDA2R) by p53 in a variety of cell types and tissues. We demonstrate that treatment of cancer cells with the ligand EDA-A2, known to specifically activate EDA2R, results in p53-dependent cell death. Moreover, we show that EDA2R is transactivated by p53 during chemotherapy-induced hair-loss, although its presence is not necessary for this process. These data shed new light on the role of EDA2R in exerting p53 function.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alopecia / genetics*
  • Cell Death / genetics
  • Gene Expression Regulation
  • Genes, p53 / genetics*
  • Transcriptional Activation*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / physiology*
  • Xedar Receptor / metabolism*

Substances

  • Tumor Suppressor Protein p53
  • Xedar Receptor