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      The levels of epithelial anchor proteins β-catenin and zona occludens-1 are altered by E7 of human papillomaviruses 5 and 8.

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          Abstract

          Infection with viruses of the genus Betapapillomavirus, β-human papillomaviruses (β-HPV), is implicated in the development of non-melanoma skin cancer. This was first evidenced for HPV5 and HPV8 in patients with the skin disease epidermodysplasia verruciformis (EV). The relocalization of the junctional bridging proteins β-catenin and zona occludens-1 (ZO-1) from the adherens and tight junctions are common processes of the epithelial-mesenchymal transition (EMT) associated with tumour invasion. Here, we report that β-catenin and ZO-1 are strongly upregulated by the E7 oncoproteins of HPV5 and HPV8 in keratinocytes grown in organotypic skin cultures. Although the membrane-tethered form of β-catenin was elevated, no signs of β-catenin activity within the canonical Wnt signalling pathway could be detected. The upregulation of β-catenin and ZO-1 could also be confirmed in the skin of HPV8 transgenic mice as well as in cutaneous squamous cell carcinomas of EV patients. These data provide the first evidence that β-catenin and ZO-1 are direct targets of E7 of the oncogenic β-HPV types 5 and 8. The ability to deregulate these epithelial junction proteins may contribute to the oncogenic potential of these viruses in human skin.

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          Author and article information

          Journal
          J. Gen. Virol.
          The Journal of general virology
          Microbiology Society
          1465-2099
          0022-1317
          Feb 2016
          : 97
          : 2
          Affiliations
          [1 ] 1​Institute of Virology, University of Cologne, Cologne, Germany.
          [2 ] 2​Department of Urology, University Hospital Cologne, Cologne, Germany.
          [3 ] 3​Department of Dermatology and Venereology, Medical University in Warsaw, Warsaw, Poland.
          Article
          10.1099/jgv.0.000363
          26645068
          16a8f689-bff4-4bf1-8bc1-fec71c1cb559
          History

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