c-Jun regulates eyelid closure and skin tumor development through EGFR signaling

Rainer Zenz, Harald Scheuch, Paul Martin, Carsten Frank, Robert Eferl, Lukas Kenner, Maria Sibilia, Erwin F Wagner

Research output: Contribution to journalArticle (Academic Journal)peer-review

222 Citations (Scopus)


To investigate the function of c-Jun during skin development and skin tumor formation, we conditionally inactivated c-jun in the epidermis. Mice lacking c-jun in keratinocytes (c-jun(Deltaep)) develop normal skin but express reduced levels of EGFR in the eyelids, leading to open eyes at birth, as observed in EGFR null mice. Primary keratinocytes from c-jun(Deltaep) mice proliferate poorly, show increased differentiation, and form prominent cortical actin bundles, most likely because of decreased expression of EGFR and its ligand HB-EGF. In the absence of c-Jun, tumor-prone K5-SOS-F transgenic mice develop smaller papillomas, with reduced expression of EGFR in basal keratinocytes. Thus, using three experimental systems, we show that EGFR and HB-EGF are regulated by c-Jun, which controls eyelid development, keratinocyte proliferation, and skin tumor formation.

Original languageEnglish
Pages (from-to)879-89
Number of pages11
JournalDevelopmental Cell
Issue number6
Publication statusPublished - Jun 2003


  • Animals
  • Apoptosis
  • Carcinogens
  • Cell Division
  • Epidermal Growth Factor
  • Epidermis
  • Eyelids
  • Gene Expression Regulation, Developmental
  • Gene Expression Regulation, Neoplastic
  • Genes, jun
  • Genetic Predisposition to Disease
  • Intercellular Signaling Peptides and Proteins
  • Mice
  • Mice, Transgenic
  • Models, Biological
  • Papilloma
  • Receptor, Epidermal Growth Factor
  • Signal Transduction
  • Skin Neoplasms
  • Tetradecanoylphorbol Acetate
  • Transgenes


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