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Fibroblast growth factor and insulin-like growth factor differentially modulate the apoptosis and G1 arrest induced

B Liu1, M Fang, Y Lu

  • 1Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas, TX 77030, USA.

Oncogene
|April 21, 2001
PubMed

Insights

Basic fibroblast growth factor (bFGF) and insulin-like growth factor-1 (IGF-1) differentially regulate apoptosis in colon cancer cells. bFGF sustained protection via the MAPK pathway, while IGF-1 offered temporary protection through PI-3K/Akt.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • DiFi human colon carcinoma cells utilize a transforming growth factor-alpha (TGF-alpha)/epidermal growth factor (EGF) receptor autocrine loop.
  • Monoclonal antibody (mAb) 225 blocks EGF receptor activation, inducing G1 arrest and apoptosis in DiFi cells.

Purpose of the Study:

  • Investigate how basic fibroblast growth factor (bFGF) and insulin-like growth factor-1 (IGF-1) influence mAb 225-induced G1 arrest and apoptosis.
  • Elucidate the specific signaling pathways modulated by bFGF and IGF-1 in this context.

Main Methods:

  • Treatment of DiFi cells with mAb 225, bFGF, and IGF-1.
  • Assessment of cell cycle arrest (G1), apoptosis, and activation of signaling pathways (MAPK, PI-3K/Akt).
  • Utilized pathway-specific inhibitors (PD98059 for MEK/MAPK, LY294002 for PI-3K).

Main Results:

  • Both bFGF and IGF-1 activated the MEK/MAPK pathway; IGF-1 also activated PI-3K/Akt.
  • Both growth factors inhibited mAb 225-induced apoptosis, with bFGF providing sustained protection and IGF-1 temporary protection.
  • bFGF reversed mAb 225-induced G1 arrest markers (p27 Kip1, CDK-2 activity, Rb dephosphorylation), while IGF-1 did not.
  • bFGF's protective effects were MEK/MAPK-dependent, whereas IGF-1's were PI-3K-dependent.

Conclusions:

  • bFGF and IGF-1 differentially modulate apoptosis and cell cycle arrest induced by EGF receptor blockade in colon cancer cells.
  • The MEK/MAPK pathway mediates bFGF's sustained anti-apoptotic and cell cycle-regulating effects.
  • The PI-3K/Akt pathway mediates IGF-1's temporary anti-apoptotic effects.

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