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C-fos is required for malignant progression of skin tumors

Academic Article
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Overview

authors

  • Saez, Enrique
  • Rutberg, S. E.
  • Mueller, E.
  • Oppenheim, H.
  • Smoluk, J.
  • Yuspa, S. H.
  • Spiegelman, B. M.

publication date

  • September 1995

journal

  • Cell  Journal

abstract

  • The proto-oncogene c-fos is a major nuclear target for signal transduction pathways involved in the regulation of cell growth, differentiation, and transformation. Using the multistep skin carcinogenesis model, we have directly tested the ability of c-fos-deficient mice to develop cancer. Upon treatment with a tumor promoter, c-fos knockout mice carrying a v-H-ras transgene were able to develop benign tumors with similar kinetics and relative incidence as wild-type animals. However, c-fos-deficient papillomas quickly became very dry and hyperkeratinized, taking on an elongated, horny appearance. While wild-type papillomas eventually progressed into malignant tumors, c-fos-deficient tumors failed to undergo malignant conversion. Experiments in which v-H-ras-expressing keratinocytes were grafted onto nude mice suggest that c-fos-deficient cells have an intrinsic defect that hinders tumorigenesis. These results demonstrate that a member of the AP-1 family of transcription factors is required for the development of a malignant tumor.

subject areas

  • Animals
  • Cell Differentiation
  • Cell Transformation, Neoplastic
  • Epidermis
  • Gene Expression
  • Genes, fos
  • Genes, ras
  • Keratinocytes
  • Keratins
  • Mice
  • Mice, Nude
  • Mice, Transgenic
  • Mutation
  • Neoplasm Transplantation
  • Oncogene Protein p21(ras)
  • Papilloma
  • Skin Neoplasms
  • Time Factors
  • Transcription Factor AP-1
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Identity

International Standard Serial Number (ISSN)

  • 0092-8674

Digital Object Identifier (DOI)

  • 10.1016/0092-8674(95)90469-7

PubMed ID

  • 7545543
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Additional Document Info

start page

  • 721

end page

  • 732

volume

  • 82

issue

  • 5

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