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The EGF receptor provides an essential survival signal for SOS-dependent skin tumor development.

The EGF receptor (EGFR) is required for skin development and is implicated in epithelial tumor formation. Transgenic mice expressing a dominant form of Son of Sevenless (SOS-F) in basal keratinocytes develop skin papillomas with 100% penetrance. However, tumor formation is inhibited in a hypomorphic (wa2) and null EGFR background. Similarly, EGFR-deficient fibroblasts are resistant to transformation by SOS-F and rasV12, however, tumorigenicity is restored by expression of the anti-apoptotic bcl-2 gene. The K5-SOS-F papillomas and primary keratinocytesfrom wa2 mice display increased apoptosis, reduced Akt phosphorylation and grafting experiments imply a cell-autonomous requirement for EGFR in keratinocytes. Therefore, EGFR functions as a survival factor in oncogenic transformation and provides a valuable target for therapeutic intervention in a broader range of tumors than anticipated.

Pubmed ID: 10943841

Authors

  • Sibilia M
  • Fleischmann A
  • Behrens A
  • Stingl L
  • Carroll J
  • Watt FM
  • Schlessinger J
  • Wagner EF

Journal

Cell

Publication Data

July 21, 2000

Associated Grants

None

Mesh Terms

  • Animals
  • Apoptosis
  • Cell Transformation, Neoplastic
  • Cells, Cultured
  • Fibroblasts
  • Humans
  • Keratinocytes
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Mice, Nude
  • Mice, Transgenic
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • Papilloma
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-akt
  • Receptor, Epidermal Growth Factor
  • Signal Transduction
  • Skin Neoplasms
  • Son of Sevenless Proteins
  • ras Proteins