Role of Phospholipid Metabolites in the Cell Cycle Delay Caused by Epidermal Growth Factor at the Transition from G2-Phase to Mitosis in A431 Cells

  • M. Kaszkin
  • V. Kinzel
Part of the Developments in Oncology book series (DION, volume 71)


In the intact organism epidermal growth factor (EGF) may not only act as a mitogen but may also participate in the control of growth, as indicated by the inhibition of replicating cells, the promotion of differentiation and other evidence (1–5). The bimodal action of EGF interferes with the cell cycle mainly at the physiological restriction points in G0/G1 or prior to mitosis in G2 (6,7). We have shown that EGF in various receptor-carrying cells including A431 cells rapidly induces a delay in the progress from G2-phase to mitosis (8). This system, therefore, may serve as a model to study mechanisms by which cells are restricted physiologically at the G2-M-border. The data obtained with A431 cells reinforce the important role physiological metabolites may play in the concert of metabolic changes required to effect cell cycle inhibition.


Epidermal Growth Factor A431 Cell Phosphatidic Acid Phosphatidic Acid Cell Cycle Delay 
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Copyright information

© Springer Science+Business Media New York 1993

Authors and Affiliations

  • M. Kaszkin
    • 1
  • V. Kinzel
    • 1
  1. 1.Department of PathochemistryDeutsches KrebsforschungszentrumHeidelbergGermany

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