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A link between cyclin A expression and adhesion-dependent cell cycle progression

T M Guadagno1, M Ohtsubo, J M Roberts

  • 1Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032.

Science (New York, N.Y.)
|December 3, 1993
PubMed
Summary
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Cell adhesion regulates cell cycle progression by controlling cyclin A expression. Loss of this control, seen in cancer, involves cyclin A bypassing adhesion signals to drive cell division.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Cell adhesion is crucial for regulating normal cell proliferation, particularly during the G1 phase of the cell cycle.
  • Loss of cell adhesion requirements is a hallmark of oncogenic transformation and cancer development.

Purpose of the Study:

  • To investigate the role of cell adhesion in regulating cell cycle progression.
  • To identify specific cell cycle regulators affected by cell adhesion in fibroblasts.
  • To determine if cyclin A is a mediator of adhesion-dependent cell proliferation control.

Main Methods:

  • Studied NRK and NIH 3T3 fibroblasts to assess cell cycle gene expression.
  • Analyzed the dependence of cyclin A, Cdc2, Cdk2, cyclin D1, and cyclin E expression on cell adhesion.

Related Experiment Videos

  • Utilized complementary DNA transfection to express cyclin A in NRK cells and evaluated its effects on proliferation.

    • Main Results:

    • Cell adhesion regulated the expression of cyclin A mRNA and protein in late G1 phase.
    • Expression of Cdc2, Cdk2, cyclin D1, and cyclin E was independent of cell adhesion.
    • Transfection with cyclin A complementary DNA led to adhesion-independent cyclin A accumulation and kinase activity, promoting cell division.

    Conclusions:

    • Cyclin A is a key target of adhesion-dependent signaling pathways that control cell proliferation.
    • Altered cyclin A regulation contributes to the loss of proliferation control observed in oncogenic transformation.