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Transformation by ras modifies AP1 composition and activity

F Mechta1, D Lallemand, C M Pfarr

  • 1Unité des Virus Oncogenes, URA 1644 du CNRS, Département des Biotechnologies, Institut Pasteur, Paris, France.

Oncogene
|February 20, 1997
PubMed

Insights

Ras proteins regulate cell growth; mutations cause abnormal proliferation. This study shows cJun and Fra1 are key mediators in Ras-driven cell transformation, linking Ras signaling to AP1 activity.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Oncology

Background:

  • Ras proteins are critical regulators of cell growth and proliferation.
  • Mutations in Ras genes are frequently observed in various human cancers, leading to uncontrolled cell division.
  • Activating Protein 1 (AP1) transcription factor activity is implicated in cellular transformation processes.

Purpose of the Study:

  • To investigate the relationship between AP1 activity and Ras-mediated cellular transformation.
  • To identify specific AP1 components involved in the transformation process induced by Ras oncogenes.

Main Methods:

  • Utilized NIH3T3 fibroblast cell clones overexpressing Ha-Ras or Ki-Ras oncogenes.
  • Analyzed protein levels of AP1 family members (Jun and Fos) and their DNA binding activity.
  • Assessed the impact of ectopic co-expression of cJun and Fra1 on NIH3T3 cell phenotype and signaling pathways.

Main Results:

  • Ras-transformed fibroblasts exhibited elevated levels of cJun, JunB, Fra1, and Fra2 proteins.
  • Increased AP1 DNA binding activity was observed, primarily involving cJun/Fra1 dimers.
  • Ectopic expression of cJun and Fra1 induced a transformed phenotype, mimicking oncogenic Ras effects.

Conclusions:

  • cJun and Fra1 are crucial mediators of Ras-driven cellular transformation.
  • Ras signaling directly impacts AP1 activity and composition, contributing to oncogenesis.
  • Specific AP1 dimers play a significant role in the abnormal proliferation characteristic of Ras-transformed cells.

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