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Related Experiment Videos

c-Myc overexpression uncouples DNA replication from mitosis.

Q Li1, C V Dang

  • 1Program in Cellular and Molecular Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

Molecular and Cellular Biology
|July 20, 1999
PubMed
Summary

Overexpression of c-myc in cells treated with colcemid leads to polyploidy or apoptosis. This suggests c-myc activation contributes to genomic instability in cancer.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • The c-myc protein regulates the G(1)/S transition phase of the cell cycle.
  • Its role in other cell cycle phases remains largely unidentified.
  • Colcemid treatment induces mitotic spindle checkpoint activation and metaphase arrest.

Purpose of the Study:

  • To investigate the role of c-myc in cell cycle phases beyond G(1)/S.
  • To determine the effects of c-myc overexpression on cells arrested in mitosis.
  • To explore the link between c-myc, cell cycle progression, and genomic instability.

Main Methods:

  • Overexpression of c-myc in human and rodent cell lines.
  • Colcemid treatment to induce cell cycle arrest.
  • Analysis of polyploidy, apoptosis, and DNA replication.

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  • Assessment of p53 status in different cell types.

    • Main Results:

    • Overexpression of c-myc induced polyploidy or apoptosis in colcemid-treated cells.
    • c-myc overexpression led to DNA replication without chromosomal segregation.
    • Primary fibroblasts exhibited massive apoptosis, while immortalized cells showed polyploidy, suggesting altered apoptotic pathways.
    • c-myc appears to induce DNA rereplication in a G(1)-like state by activating CDK2.

    Conclusions:

    • c-myc plays a role in cell cycle progression beyond G(1)/S, influencing mitosis and G(1)-like states.
    • Activation of c-myc can lead to genomic instability through polyploidy and DNA rereplication.
    • The p53 status and other genetic alterations influence the cellular response (apoptosis vs. polyploidy) to c-myc overexpression during cell cycle arrest.