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HPV8 activates cellular gene expression mainly through Sp1/3 binding sites

Matthias Kirschberg1, Sandra Heuser1, Adnan S Syed1

  • 1Institute of Virology, University of Cologne, Faculty of Medicine and University Hospital of Cologne, Germany.

Virology
|July 13, 2019
PubMed

Insights

Human papillomavirus type 8 (HPV8) oncoproteins, particularly HPV8-E7, influence skin gene expression via Sp1/3 binding sites. This mechanism contributes to HPV8-associated skin cancer development and fibronectin-dependent cell invasion.

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Human papillomavirus type 8 (HPV8) is linked to skin cancer.
  • Understanding HPV8 oncoproteins' role in gene regulation is crucial for cancer research.

Purpose of the Study:

  • Investigate HPV8 oncoprotein effects on cellular gene expression.
  • Identify key regulators of HPV8-mediated gene expression changes.
  • Elucidate the role of fibronectin in HPV8-associated skin cancer.

Main Methods:

  • Affymetrix microarray analysis to identify differentially expressed genes.
  • Transient transfection assays to assess promoter activity.
  • Analysis of skin models and HPV8-positive skin cancers for fibronectin deposition and protein correlation.

Main Results:

  • HPV8-E7 activates Sp1/3 promoters, indicating Sp1/3 binding sites are crucial regulators.
  • A specific HPV8-E7 mutant (L23A) failed to activate fibronectin gene expression, suggesting its role in invasion.
  • Fibronectin deposition was observed in the dermal compartment of skin models and HPV8-positive cancers.
  • Correlation between Sp3 and fibronectin was found in the nucleus of HPV8-positive keratinocytes.

Conclusions:

  • HPV8-E7 controls cellular gene expression through Sp1/3 binding motifs.
  • This regulation contributes to HPV8-mediated keratinocyte transformation.
  • Fibronectin plays a role in HPV8-associated cell invasion.
Keywords:
Epidermodysplasia verruciformisFibronectinHuman papillomavirusOrganotypic skin cultureSP1/3Transcription

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