Generation of K14-E7/∆N87βcat double transgenic mice as a model of cervical cancer

Methods Mol Biol. 2015:1249:393-406. doi: 10.1007/978-1-4939-2013-6_29.

Abstract

Nearly all cervical cancers are initiated by a subset of high-risk human papilloma viruses (HPVs). However, cervical cancers develop only in a small fraction of women who are infected with these viruses. HPV is required, but not sufficient for developing cervical cancer. Activation of complementary signaling pathways appears to be necessary for malignant transformation of cervical epithelial cells that are immortalized by HPV. Here, we describe the creation and maintenance of a double transgenic mouse model that is based on constitutively active Wnt/β-catenin signaling in cervical epithelial cells expressing the HPV oncoprotein E7. These mice develop invasive cervical squamous carcinomas within 6 months with an average penetrance of 94 %.

Publication types

  • Research Support, American Recovery and Reinvestment Act
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Breeding
  • Disease Models, Animal*
  • Estradiol / pharmacology
  • Female
  • Genetic Techniques*
  • Genotyping Techniques
  • Humans
  • Keratin-14 / genetics
  • Keratin-14 / metabolism*
  • Mice, Transgenic
  • Necrosis
  • Papillomavirus E7 Proteins / metabolism*
  • Paraffin Embedding
  • Uterine Cervical Neoplasms / pathology*
  • beta Catenin / metabolism*

Substances

  • Keratin-14
  • Papillomavirus E7 Proteins
  • beta Catenin
  • oncogene protein E7, Human papillomavirus type 16
  • Estradiol