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Updated: Oct 2, 2026

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

Dominant negative interference of transcription factor AP-2 causes inhibition of ErbB-3 expression and suppresses

Chun-Hong Zhu1, Frederick E Domann

  • 1Free Radical & Radiation Biology Program, Department of Radiation Oncology, and Holden Comprehensive Cancer Center, The University of Iowa, Iowa City 52242, USA.

Breast Cancer Research and Treatment
|February 28, 2002
PubMed

Insights

Transcription factor AP-2gamma (also known as activating enhancer-binding protein 2 gamma) regulates ErbB-3 (also known as HER3) expression. This suggests AP-2 family proteins may be therapeutic targets for reducing malignancy.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • ErbB-3 (HER3) is a receptor tyrosine kinase implicated in cancer malignancy.
  • The transcription factor AP-2 family plays a role in regulating gene expression.

Purpose of the Study:

  • To investigate the role of the AP-2 transcription factor family in regulating ErbB-3 expression.
  • To explore the potential of targeting AP-2 for cancer therapy.

Main Methods:

  • Analysis of ErbB-3 expression in human mammary epithelial and fibroblast cell lines.
  • Co-transfection experiments to assess AP-2gamma's effect on ErbB-3 promoter activity.
  • Use of a dominant-negative AP-2 mutant to study endogenous ErbB-3 transcription.
  • Cell proliferation and colony formation assays.

Main Results:

  • Elevated ErbB-3 expression correlated with AP-2gamma presence, but not AP-2alpha or AP-2beta.
  • AP-2gamma robustly activated the ErbB-3 promoter.
  • A dominant-negative AP-2 mutant repressed ErbB-3 promoter activity and transcription.
  • AP-2gamma overexpression reduced cell proliferation and colony formation.

Conclusions:

  • The AP-2 gene family, particularly AP-2gamma, plays a crucial role in controlling ErbB-3 expression.
  • Targeting AP-2 function offers a potential strategy for modulating malignant phenotypes by controlling ErbB-3 levels.

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