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Negative growth regulation of SK-N-MC cells by bFGF defines a growth factor-sensitive point in G2

V A Smits1, M A van Peer, M A Essers

  • 1Jordan Laboratory, Department of Hematology, University Medical Center Utrecht G03.647, P.O. Box 85500, 3508 GA Utrecht, The Netherlands.

The Journal of Biological Chemistry
|April 20, 2000
PubMed

Insights

Basic fibroblast growth factor (bFGF) inhibits neuroepithelioma cell growth in G2 phase, an unusual mechanism. This involves bFGF impacting cdc2 phosphorylation and Cdc25C activation, similar to DNA damage responses.

Area of Science:

  • Cell cycle regulation
  • Molecular biology
  • Cancer research

Background:

  • Basic fibroblast growth factor (bFGF) is known to inhibit the growth of the SK-N-MC neuroepithelioma cell line.
  • Cellular responses to extracellular signals are typically thought to cease after the restriction point in the cell cycle.

Purpose of the Study:

  • To investigate the mechanism by which bFGF induces growth inhibition in SK-N-MC cells.
  • To identify the specific phase of the cell cycle affected by bFGF and the molecular players involved.

Main Methods:

  • Cell cycle analysis of SK-N-MC cells treated with bFGF.
  • Western blot analysis to assess cdc2 phosphorylation and Cdc25C activation.
  • Generation and use of tetracycline-regulatable SK-N-MC clones expressing a Cdc25C mutant (Cdc25C-S216A).

Main Results:

  • bFGF induces growth inhibition specifically during the G2 phase of the cell cycle.
  • bFGF treatment inhibits Tyr-15 dephosphorylation of cdc2 and prevents Cdc25C activation, mimicking DNA damage responses.
  • Caffeine treatment reverses both bFGF- and DNA damage-induced effects on cdc2 phosphorylation.
  • Expression of Cdc25C-S216A rescues cells from bFGF-induced G2 block and normalizes cdc2 phosphorylation.

Conclusions:

  • A novel growth factor-sensitive regulatory point exists in the G2 phase of the cell cycle.
  • This G2 regulation likely involves the phosphorylation status of Cdc25C.
  • bFGF utilizes pathways similar to DNA damage response pathways to control cell cycle progression.

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