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Insulin-like growth factor I receptor signaling in transformation by src oncogenes

B Valentinis1, A Morrione, S J Taylor

  • 1Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

Molecular and Cellular Biology
|July 1, 1997
PubMed

Insights

Mouse embryo fibroblasts lacking insulin-like growth factor I (IGF-I) receptors can be transformed by v-src oncogene, but not c-src527. This suggests v-src bypasses IGF-I receptor signaling for cell transformation.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Signal Transduction

Background:

  • Mouse embryo fibroblasts with disrupted insulin-like growth factor I (IGF-I) receptor genes (R- cells) are resistant to oncogene-induced transformation.
  • Understanding the role of IGF-I receptor signaling in cell transformation is crucial for cancer research.

Purpose of the Study:

  • To investigate the differential transformation capabilities of v-src and c-src527 oncogenes in R- cells.
  • To identify signaling pathways that mediate cell transformation independently of IGF-I receptor function.

Main Methods:

  • Transformation assays using colony formation in soft agar.
  • Analysis of tyrosine phosphorylation of key signaling proteins, including focal adhesion kinase, Stat1, and p130cas.
  • Comparison of v-src and c-src527 oncogene activity in R- cells versus wild-type cells.

Main Results:

  • R- cells were transformed by v-src, but not by activated c-src527, indicating v-src can bypass the need for a functional IGF-I receptor.
  • v-src demonstrated greater efficiency in phosphorylating focal adhesion kinase, Stat1, and p130cas in R- cells compared to c-src527.
  • Differences in substrate phosphorylation did not fully explain the observed transformation differences, suggesting complex signaling mechanisms.

Conclusions:

  • v-src, unlike c-src527, can induce full transformation of mouse embryo fibroblasts by circumventing IGF-I receptor signaling.
  • Qualitative and quantitative differences between v-src and c-src527 highlight specific oncogenic signals relevant to transformation mechanisms.
  • These findings provide insights into alternative pathways driving cell transformation and cancer development.

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