EGR-1, a UV-inducible gene in p53(-/-) mouse cells

Exp Cell Res. 2001 May 15;266(1):21-30. doi: 10.1006/excr.2001.5196.

Abstract

Changes in gene expression were examined in p53(-/-) and p53(+/+) mouse cells after ultraviolet (UV) irradiation. Differential display was used to identify differentially expressed gene(s) in UV-treated p53(-/-) and p53(+/+) cells. One of the differentially expressed genes was EGR-1 (early growth response gene-1), which was shown to be induced only in p53(-/-) cells. The induction of this gene by UV was detected as early as 0.5 h, peaked at 2 h, and returned to normal levels by 4 h. De novo protein synthesis was not required for UV-induced EGR-1 expression in p53(-/-) cells. Pretreatment of p53(-/-) cells with suramin, an inhibitor of growth factor receptors, completely suppressed UV-induced EGR-1 expression, suggesting that the induction may be mediated via the growth factor receptors. The presence of wild-type p53 suppressed the induction of EGR-1 after UV treatment. Overexpression of EGR-1 promoted the UV-induced transformation in p53(+/+) cells, but not in p53(-/-) cells. These data suggested that EGR-1 may be an important player in the UV responses of mammalian cells and may influence UV-induced transformation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Cell Line, Transformed / drug effects
  • Cell Line, Transformed / metabolism
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Early Growth Response Protein 1
  • Gene Expression Regulation, Neoplastic / genetics*
  • Immediate-Early Proteins*
  • Mice
  • Mice, Knockout / genetics
  • Mice, Knockout / metabolism
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Neoplasms / physiopathology
  • Receptors, Growth Factor / drug effects
  • Receptors, Growth Factor / metabolism
  • Suramin / pharmacology
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism
  • Tumor Suppressor Protein p53 / deficiency*
  • Tumor Suppressor Protein p53 / genetics*
  • Ultraviolet Rays / adverse effects*

Substances

  • Antineoplastic Agents
  • DNA-Binding Proteins
  • Early Growth Response Protein 1
  • Egr1 protein, mouse
  • Immediate-Early Proteins
  • Receptors, Growth Factor
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Suramin