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Transforming growth factor beta 1-mediated growth inhibition in chick embryo fibroblasts: reversion by

F Piu1, P Jurdic, G Brun

  • 1Laboratoire de Biologie Moléculaire et Cellulaire, Ecole Normale Supérieure, UMR 49, CNRS, 46, Lyon, France.

Comptes Rendus De L'Academie Des Sciences. Serie III, Sciences De La Vie
|August 1, 1993
PubMed

Insights

Transforming growth factor beta 1 (TGF-beta 1) inhibits cell growth, but oncogenes like v-jun and v-myc can reverse this effect. These findings suggest interactions between TGF-beta 1 and oncogene pathways involving transcription factors.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Transforming growth factor beta 1 (TGF-beta 1) is a key regulator of cell growth.
  • Oncogenes play critical roles in cell proliferation and cancer development.

Purpose of the Study:

  • To investigate the interaction between TGF-beta 1-induced growth inhibition and oncogene-mediated cell stimulation.
  • To identify the molecular players involved in these opposing pathways.

Main Methods:

  • Primary cultures of chick embryo fibroblasts were used.
  • The effects of TGF-beta 1 and various nuclear oncogenes (v-jun, v-fos, v-myc, v-erbA, v-ets, v-myb) on cell growth and generation time were assessed.

Main Results:

  • TGF-beta 1 inhibited fibroblast growth by affecting the G1 phase and increasing generation time.
  • Oncogenes v-jun, v-fos, v-myc, and v-myb reversed TGF-beta 1-induced growth inhibition.
  • Oncogenes v-erbA and v-ets did not reverse the inhibition.

Conclusions:

  • TGF-beta 1 and oncogene-driven growth stimulatory pathways can functionally interfere with each other.
  • This interference likely occurs at the level of transcription factors, specifically AP-1, Myc, and Myb.

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