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Deregulated cell cycle control in lens epithelial cells by expression of inhibitors of tumor suppressor function

Minh M Nguyen1, Sarah J Potter, Anne E Griep

  • 1Department of Anatomy, The University of Wisconsin Medical School, 1300 University Avenue, Madison, WI 53706, USA.

Mechanisms of Development
|February 19, 2002
PubMed

Insights

Cell cycle control in the lens epithelium involves multiple factors, including the retinoblastoma protein (pRB) family. Oncogenes E6 and E7 from human papillomavirus type 16 were used to study lens cell proliferation.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Genetics

Background:

  • Cell cycle proteins like retinoblastoma protein (pRB) are crucial for lens cell differentiation.
  • The specific factors governing cell cycle control in lens epithelial cells remain largely uncharacterized.

Purpose of the Study:

  • To investigate the role of specific cell cycle regulators in lens epithelial cell proliferation.
  • To utilize human papillomavirus type 16 (HPV16) oncogenes as molecular tools to probe lens cell cycle control.

Main Methods:

  • Generation of transgenic mice expressing HPV16 E6 or E7 oncogenes under the K14 promoter.
  • Analysis of lens phenotypes, including cell proliferation, apoptosis, and tissue morphology.
  • Assessment of p53 and pRB inactivation by E6 and E7, and the impact of E7 mutants.

Main Results:

  • Expression of E6 or E7 led to increased proliferation and apoptosis in the lens epithelium.
  • E6 expression induced a distinct epithelial phenotype with multilayering and intercellular vacuoles.
  • The observed lens phenotype in E6 mice was independent of p53, and E7 mutants defective in pRB inactivation did not cause abnormalities.

Conclusions:

  • Cell proliferation in the lens epithelium is regulated by multiple factors, with the pRB family playing a significant role.
  • HPV16 E6 and E7 oncogenes serve as valuable tools for dissecting cell cycle regulation in the lens.
  • Lens cell cycle control is a complex process involving more than just p53 and pRB pathways.

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