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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

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Transcription factor AP-2gamma stimulates proliferation and apoptosis and impairs differentiation in a transgenic

Richard Jäger1, Uwe Werling, Stephan Rimpf

  • 1Institute for Pathology, Department of Developmental Pathology, University of Bonn Medical School, Bonn, Germany.

Molecular Cancer Research : MCR
|October 24, 2003
PubMed

Insights

AP-2 transcription factors influence cell growth and development. Overexpressing AP-2gamma in mice disrupted mammary gland and seminal vesicle development, suggesting a role in cell proliferation and tumorigenesis.

Area of Science:

  • Developmental Biology
  • Cancer Biology
  • Molecular Endocrinology

Background:

  • AP-2 transcription factors are crucial for embryonic development, regulating cell differentiation, proliferation, and survival.
  • Aberrant AP-2 activity is linked to carcinogenesis, indicating a role in disrupted cellular growth programs.

Purpose of the Study:

  • To investigate the role of AP-2 transcription factors, specifically AP-2gamma, in mammary gland tumorigenesis.
  • To elucidate the effects of AP-2gamma overexpression on mammary gland and seminal vesicle development and function.

Main Methods:

  • Generation of transgenic mice overexpressing AP-2gamma using the mouse mammary tumor virus-long terminal repeat promoter.
  • Analysis of mammary gland and seminal vesicle tissues for proliferation, apoptosis, differentiation, and gene expression changes.
  • Assessment of androgen receptor immunoreactivity in male transgenic mice.

Main Results:

  • AP-2gamma overexpression in mammary glands led to hyperproliferation counterbalanced by increased apoptosis, resulting in hypoplasia and impaired secretory differentiation.
  • In male mice, AP-2gamma overexpression in seminal vesicles caused pronounced effects on proliferation and apoptosis, alongside impaired differentiation indicated by absent androgen receptor.
  • Elevated IGFBP-5 transcript levels, an AP-2 target gene, were observed in both tissues, suggesting a mechanism for AP-2-induced apoptosis.

Conclusions:

  • AP-2 transcription factors promote a proliferative and undifferentiated cellular state.
  • These findings highlight a significant role for AP-2 in maintaining cellular characteristics relevant to both embryonic development and tumorigenesis.

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