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Cell cycle re-entry following chemically-induced cell cycle synchronization leads to elevated p53 and p21 protein

C Ji1, L J Marnett, J A Pietenpol

  • 1Department of Biochemistry, Center in Molecular Toxicology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0146, USA.

Oncogene
|December 24, 1997
PubMed

Insights

Cell synchronization agents like mimosine (MIM) and aphidicolin (APH) can alter p53 and p21 protein levels, impacting cell cycle studies. Researchers should use caution when interpreting results from synchronized cells, especially in p53/p21 pathway investigations.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Mimosine (MIM) and aphidicolin (APH) are common agents for synchronizing cells in late G1 and S phases.
  • These agents are frequently employed in tissue culture experiments to study cell cycle regulation.

Purpose of the Study:

  • To investigate the effects of MIM and APH on p53 and p21 protein levels during and after cell cycle synchronization.
  • To determine if MIM and APH treatments influence the response of cells to genotoxic agents.

Main Methods:

  • Human cancer cell lines were treated with MIM or APH to induce cell cycle arrest.
  • Protein levels of p53 and p21 were analyzed during and after the release from synchronization.
  • Cells were subsequently treated with genotoxic agents to assess the impact of prior synchronization.

Main Results:

  • MIM and APH induced reversible cell cycle arrest with moderate increases in p53 and p21.
  • Both p53-dependent and -independent increases in p21 were observed.
  • A striking and sustained elevation of p53 and p21 occurred post-synchronization.
  • Prior MIM or APH treatment enhanced p21 induction by genotoxic agents.

Conclusions:

  • Cell synchronization using MIM or APH can lead to significant alterations in p53 and p21 protein levels.
  • These alterations persist after cells re-enter the cell cycle, potentially confounding experimental results.
  • Caution is advised when interpreting data from synchronized cells, particularly in studies of p53 and p21 regulatory pathways.

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