E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

Oncogene. 2000 Jan 27;19(4):592-8. doi: 10.1038/sj.onc.1203339.


In addition to their role in anogenital cancer, human papillomaviruses (HPVs) are also involved in the development of a range of cutaneous lesions. HPV types 5 and 8 are associated with the development of skin cancers in individuals with Epidermodysplasia verruciformis (EV). A broad spectrum of HPV types are also commonly found in non-melanoma skin cancers in immunocompromised individuals, such as organ transplant recipients. The skin cancers in EV and immunocompromised patients occur predominantly at body sites exposed to ultra violet (UV) radiation, pointing to a key role for UV in their development. Here we show that the E6 protein from a range of cutaneous HPV types effectively inhibits apoptosis in response to UV damage. This occurs in both p53 null and wild type cells and does not require p53 degradation.

Publication types

  • Comparative Study

MeSH terms

  • Apoptosis / physiology*
  • Apoptosis / radiation effects
  • Cell Line
  • Cell Transformation, Viral
  • Cocarcinogenesis
  • DNA Fragmentation
  • DNA-Binding Proteins*
  • Dose-Response Relationship, Radiation
  • Humans
  • Neoplasms, Radiation-Induced / etiology
  • Neoplasms, Radiation-Induced / virology
  • Oncogene Proteins, Viral / physiology*
  • Papillomaviridae / classification
  • Papillomaviridae / physiology*
  • Papillomavirus Infections / virology*
  • Polymerase Chain Reaction
  • Radiation Tolerance
  • Recombinant Fusion Proteins / physiology
  • Skin / virology*
  • Skin Neoplasms / etiology
  • Skin Neoplasms / virology
  • Tumor Suppressor Protein p53 / physiology
  • Tumor Virus Infections / virology*
  • Ultraviolet Rays*


  • DNA-Binding Proteins
  • E6 protein, Human papillomavirus type 18
  • Oncogene Proteins, Viral
  • Recombinant Fusion Proteins
  • Tumor Suppressor Protein p53