EGR1 Target Genes That Regulate Growth/Survival of Prostate Cells

Abstract

Related co-activators p3OO and CBP, affect the transcriptional activities of many transcription factors (TF), producing multiple downstream effects. I have shown that the immediate early response TF, Egr1, acts upstream of p3OO/CBP to induce or to repress transcription, depending on stimulus. Cells induced with serum to increase endogenous Egr1, increase the transcription of p3OO/CBP, only when Egr1 binding sites in the promoter are not mutated, causing the expression of downstream targets of Egr1 leading to survival. Induction of p3OO/CBP by Egr1, results in acetylation and stabilization of Egr1 and transactivation of survival genes but repression of Egr1 and p3OO/CBP in negative feedback loops. In contrast, induction of Egr1 by UV-C irradiation leads to repression of p3OO/CBP transcription: Egr1 is preferentially phosphorylated, leading to regulation of target genes that cause cell death. This complex balance of opposing effects appears to finely modulate important cellular life and death responses. I have shown that serum stimulation of prostate cells results in cell growth by the up-regulation of p3OO/CBP. In contrast, the stimulus of ultraviolet irradiation leads to cell cycle block and apoptosis through the inhibition of p3OO/CBP.

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Document Details

Document Type
Technical Report
Publication Date
Mar 01, 2004
Accession Number
ADA425989

Entities

People

  • Jianxiu Yu

Organizations

  • Sanford Burnham Prebys Medical Discovery Institute

Tags

DTIC Thesaurus Topics

  • Acetylation
  • Apoptosis
  • Cancer
  • Carrier Proteins
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Contrast
  • Feedback
  • Fibroblasts
  • Growth Factors
  • Inhibition
  • Prostate
  • Prostate Cancer
  • Proteins
  • Transcription Factors

Fields of Study

  • Biology

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