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Related Experiment Videos

Gene regulation by IGF-I

R Baserga1

  • 1Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, PA 19107-5541.

Molecular Reproduction and Development
|August 1, 1993
PubMed
Summary
This summary is machine-generated.

Overexpressing the insulin-like growth factor-I (IGF-I) receptor enables 3T3 cells to grow with EGF by increasing IGF-I production. SV40 transformation also boosts IGF-I production, reducing growth factor dependency.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • 3T3 cell growth typically requires multiple growth factors, including insulin-like growth factor-I (IGF-I), platelet-derived growth factor (PDGF), and epidermal growth factor (EGF).
  • Overexpression of specific growth factor receptors can alter cellular responses to growth stimuli.

Purpose of the Study:

  • To investigate the mechanism by which epidermal growth factor (EGF) induces growth in 3T3 cells overexpressing the insulin-like growth factor-I (IGF-I) receptor.
  • To determine the role of the IGF-I receptor in EGF-stimulated growth.
  • To examine the effect of SV40 large T antigen on IGF-I production and cell growth.

Main Methods:

  • Utilizing 3T3 cells with constitutive overexpression of the IGF-I receptor.

Related Experiment Videos

  • Treating cells with EGF and assessing growth.
  • Measuring IGF-I RNA and secreted IGF-I levels.
  • Employing a temperature-sensitive mutant of the SV40 large T antigen.
  • Using a luciferase reporter assay with an IGF-I promoter.

    • Main Results:

    • EGF induced growth in IGF-I receptor-overexpressing cells by stimulating substantial IGF-I RNA and protein production.
    • A functional IGF-I receptor was essential for growth even in cells overexpressing the EGF receptor.
    • SV40 large T antigen significantly increased IGF-I mRNA and secreted IGF-I levels.
    • Increased IGF-I expression by T-antigen occurred at least partly at the transcriptional level.

    Conclusions:

    • EGF can promote cell growth in cells overexpressing the IGF-I receptor through autocrine IGF-I production.
    • SV40 transformation appears to reduce the requirement for exogenous growth factors by upregulating endogenous IGF-I production, at least partly via transcriptional control.