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Insulin-like growth factor binding protein-3 induces apoptosis in MCF7 breast cancer cells

T Nickerson1, H Huynh, M Pollak

  • 1Lady Davis Research Institute, Jewish General Hospital, Montreal, Quebec, Canada.

Biochemical and Biophysical Research Communications
|August 28, 1997
PubMed

Insights

The antiestrogen ICI 182,780 (ICI) and insulin-like growth factor binding protein-3 (IGFBP-3) promote apoptosis in breast cancer cells. This suggests IGFBPs regulate cell death, potentially through modulating insulin-like growth factor (IGF) bioavailability.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cancer Research

Background:

  • Insulin-like growth factors (IGFs) possess significant antiapoptotic properties.
  • The antiestrogen ICI 182,780 (ICI) inhibits MCF7 human breast cancer cell growth, partly by upregulating insulin-like growth factor binding proteins (IGFBPs) -3 and -5.
  • IGFBPs typically attenuate IGF bioactivity.

Purpose of the Study:

  • To investigate the role of ICI and IGFBP-3 in inducing apoptosis in MCF7 cells.
  • To elucidate the mechanism by which IGFBP-3 and ICI influence apoptosis.
  • To determine if IGF bioactivity modulation by IGFBPs affects apoptosis.

Main Methods:

  • MCF7 cells were treated with ICI or recombinant human IGFBP-3.
  • Apoptosis was quantified using a cell death ELISA measuring DNA fragmentation.
  • The effects of IGF-I and a modified IGF-I analogue (Long R3 IGF-I) on apoptosis were compared.

Main Results:

  • Treatment with ICI or IGFBP-3 significantly increased apoptosis (approximately 3.5-fold) in MCF7 cells.
  • Long R3 IGF-I, which has reduced affinity for IGFBPs, was more effective than IGF-I in inhibiting IGFBP-3- and ICI-induced apoptosis.
  • These findings indicate that IGFBP-3 enhances apoptosis by limiting IGF bioavailability.

Conclusions:

  • ICI-induced apoptosis in MCF7 cells is partly mediated by modulation of IGFBP-3 expression.
  • IGFBP-3 promotes apoptosis by reducing the bioavailability of ligands for the IGF-I receptor.
  • The study suggests that IGFBPs generally function as regulators of apoptosis.

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