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Related Experiment Videos

A mutant p53 antagonizes the deregulated c-myc-mediated enhancement of apoptosis and decrease in leukemogenicity

J Lotem1, L Sachs

  • 1Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.

Proceedings of the National Academy of Sciences of the United States of America
|October 10, 1995
PubMed
Summary

The [Val135]p53 mutant enhanced leukemic cell apoptosis and tumor development when coexpressed with deregulated c-myc. This suggests a gain-of-function for the mutant p53 in cancer progression.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The p53 tumor suppressor protein plays a critical role in preventing cancer.
  • Mutations in p53 are common in human cancers, and some mutant forms exhibit altered functions.
  • Deregulation of c-myc is frequently observed in various cancers, promoting cell proliferation.

Purpose of the Study:

  • To investigate the functional impact of the [Val135]p53 mutant and deregulated c-myc on myeloid leukemic M1 cells.
  • To determine how coexpression of the [Val135]p53 mutant and deregulated c-myc affects apoptosis and leukemogenicity.
  • To explore potential gain-of-function properties of the [Val135]p53 mutant in a leukemic context.

Main Methods:

  • Transfection of M1 leukemic cells with constructs expressing the [Val135]p53 mutant and/or deregulated c-myc.

Related Experiment Videos

  • Assessment of autonomous cell growth, cloning efficiency, and susceptibility to apoptosis.
  • Evaluation of leukemogenicity through injection into isologous mice.

    • Main Results:

    • Constitutive expression of the [Val135]p53 mutant or deregulated c-myc did not alter the basal growth rate or cloning efficiency of M1 cells.
    • Deregulation of c-myc increased M1 cell susceptibility to apoptosis and reduced leukemogenicity.
    • The [Val135]p53 mutant alone did not affect apoptosis or leukemogenicity but suppressed the effects of deregulated c-myc, indicating a gain-of-function in this context.

    Conclusions:

    • The [Val135]p53 mutant exhibits a gain-of-function by enhancing susceptibility to apoptosis and increasing leukemogenicity when coexpressed with deregulated c-myc.
    • This gain-of-function of the mutant p53 contributes to enhanced tumor development in leukemic cells.
    • The interplay between mutant p53 and c-myc deregulation has significant implications for cancer progression and therapeutic strategies.