Protein kinase C-and ras-dependent activation of c-jun gene by human papillomavirus type 11 E5a oncoprotein

Cancer Lett. 1995 Aug 16;95(1-2):201-5. doi: 10.1016/0304-3835(95)03894-3.

Abstract

E5a of HPV-11 is a transforming oncogene. Previously, we have shown that E5a constitutively activates the expression of protooncogene c-jun by transcriptional regulation through the AP-1 binding site in the c-jun promoter. In the present study, we used two different types of cells: the E5a transfected NIH 3T3 cells and human epidermal keratinocytes, and selectively inhibited different signal transduction pathways to investigate effects of E5a on c-jun expression. We find that protein kinase C and ras-dependent pathways are important for the c-jun induction by E5a, but not the cAMP-dependent pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • 3T3 Cells
  • Animals
  • Blotting, Western
  • Cells, Cultured
  • Cyclic AMP / physiology
  • Genes, jun*
  • Humans
  • In Vitro Techniques
  • Isoquinolines / pharmacology
  • Keratinocytes / metabolism
  • Mice
  • Oncogene Proteins, Viral / physiology*
  • Papillomaviridae / physiology*
  • Piperazines / pharmacology
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism*
  • Proto-Oncogene Proteins c-jun / metabolism*
  • Proto-Oncogene Proteins p21(ras) / metabolism*
  • Signal Transduction
  • Sulfonamides*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transfection

Substances

  • E5A protein, Human papillomavirus type 11
  • Isoquinolines
  • Oncogene Proteins, Viral
  • Piperazines
  • Proto-Oncogene Proteins c-jun
  • Sulfonamides
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • N-(2-guanidinoethyl)-5-isoquinolinesulfonamide
  • Cyclic AMP
  • Protein Kinase C
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)
  • Tetradecanoylphorbol Acetate