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Regulation of the insulin-like growth factor-I receptor gene by oncogenes and antioncogenes: implications in human

H Werner1, M Shalita-Chesner, S Abramovitch

  • 1Department of Clinical Biochemistry, Tel Aviv University, Tel Aviv, 69978, Israel. hwerner@post.tau.ac.il

Molecular Genetics and Metabolism
|September 26, 2000
PubMed

Insights

Tumor suppressors like WT1 and p53 inhibit insulin-like growth factor-I receptor (IGF-I-R) gene activity, while oncogenes stimulate it. This balance regulates cell proliferation and transformation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The insulin-like growth factor-I receptor (IGF-I-R) is crucial for cell growth and cancer development.
  • Tumor suppressor genes (e.g., WT1, p53, BRCA1) and oncogenes influence IGF-I-R gene expression.
  • Dysregulation of IGF-I-R signaling is implicated in various cancers.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling IGF-I receptor gene transcription.
  • To elucidate the roles of specific tumor suppressors and oncogenes in modulating IGF-I-R promoter activity.
  • To understand how the interplay between transcription factors impacts cellular proliferation.

Main Methods:

  • Analysis of IGF-I receptor gene promoter activity.
  • Investigation of transcription factor binding and function.
  • Assessment of cell-surface IGF binding levels.

Main Results:

  • Wild-type tumor suppressors (WT1, p53, BRCA1) suppress IGF-I-R promoter activity.
  • Oncogenes (mutant p53, c-myb) and EWS-WT1 fusion protein stimulate IGF-I-R promoter activity.
  • Differential regulation by transcription factors affects IGF-I-R expression and cell proliferation.

Conclusions:

  • The expression of the IGF-I receptor is tightly controlled by a balance of stimulatory and inhibitory transcription factors.
  • Understanding these regulatory interactions is key to comprehending cell proliferation and transformation processes.
  • Targeting IGF-I-R signaling pathways holds potential for cancer therapy.

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