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Requirement of epidermal growth factor receptor for hyperplasia induced by E5, a high-risk human papillomavirus

Sybil M Genther Williams1, Gary L Disbrow, Richard Schlegel

  • 1McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.

Cancer Research
|August 3, 2005
PubMed

Insights

Human papillomavirus (HPV) E5 oncoprotein drives epithelial tumors in mice by altering cell growth and differentiation. This study demonstrates the epidermal growth factor receptor is essential for E5-induced hyperplasia.

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Cellular signaling pathways are crucial for multicellular organism development and homeostasis.
  • Dysregulation of these pathways can lead to diseases like cancer.
  • High-risk human papillomaviruses (HPVs) are linked to cancer and can manipulate cellular signaling.

Purpose of the Study:

  • To investigate the role of HPV16 E5 oncogene in epithelial carcinogenesis.
  • To generate and analyze a transgenic mouse model expressing HPV16 E5 in stratified squamous epithelium.
  • To determine the mechanism by which E5 alters epithelial growth and differentiation.

Main Methods:

  • Generation of transgenic mice expressing the HPV16 E5 gene in the basal layer of stratified squamous epithelium.
  • Characterization of epithelial alterations, including growth and differentiation.
  • Analysis of the role of epidermal growth factor receptor (EGFR) in E5-mediated effects.

Main Results:

  • Transgenic mice expressing HPV16 E5 developed epithelial tumors at a high frequency.
  • E5 expression led to significant alterations in stratified epithelial growth and differentiation.
  • The study identified a requirement for the epidermal growth factor receptor in mediating E5's hyperplastic effects.

Conclusions:

  • The HPV16 E5 oncogene can induce epithelial tumors in vivo.
  • E5 modulates epithelial cell growth and differentiation, contributing to oncogenesis.
  • Epidermal growth factor receptor signaling is critical for the hyperplastic activity of HPV16 E5.

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