Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

c-Myc functionally cooperates with Bax to induce apoptosis.

Philippe Juin1, Abigail Hunt, Trevor Littlewood

  • 1University of California at San Francisco Cancer Center, San Francisco, California 94143-0128, USA.

Molecular and Cellular Biology
|August 9, 2002
PubMed
Summary

The oncogene c-Myc induces programmed cell death (apoptosis) by disrupting mitochondria. This process requires the protein Bax, but c-Myc does not alter Bax levels, suggesting an indirect mechanism.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Corrigendum: Inhibition of Myc family proteins eradicates KRas-driven lung cancer in mice.

Genes & development·2026
Same author

NOXA/MCL-1 axis determines cell-death decision between apoptosis and a GSDME-dependent cell death associated with production of inflammatory cytokines upon treatment of breast cancer cells with antimitotics.

Cell death & disease·2026
Same author

Peripheral blood transcriptional profiling predicts tumor subtype and neoadjuvant chemoimmunotherapy outcomes in human breast cancer.

Science translational medicine·2026
Same author

Hallmarks of Cancer: How did it inspire you?

Cell·2026
Same author

Long-term outcomes of elosulfase alfa enzyme replacement therapy in adults with MPS IVA: a sub-analysis of the Morquio A Registry Study (MARS).

Orphanet journal of rare diseases·2025
Same author

Real-world treatment with elosulfase alfa in patients with MPS IVA is associated with improved endurance over time.

Genetics in medicine open·2025

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Biochemistry

Background:

  • c-Myc is a transcription factor known to regulate cell proliferation, differentiation, and apoptosis.
  • Mitochondrial integrity is crucial for regulating cell death pathways, with proteins like Bcl-2 family members playing key roles.
  • The precise mechanisms by which c-Myc induces apoptosis, particularly its interaction with the Bcl-2 family, are not fully understood.

Purpose of the Study:

  • To elucidate the role of Bcl-2 family proteins, specifically Bax and Bak, in c-Myc-induced apoptosis.
  • To investigate how c-Myc activation influences Bax expression, localization, and conformation.
  • To determine if direct activation of proapoptotic pathways can rescue c-Myc-induced apoptosis in resistant cells.

Main Methods:

Related Experiment Videos

  • Utilized knockout fibroblasts lacking Bak or Bax to assess susceptibility to c-Myc-induced apoptosis.
  • Analyzed Bax expression, localization, and conformation following c-Myc activation.
  • Employed ectopic expression of Bax and microinjection of a BH3-only domain peptide to restore apoptosis sensitivity.
  • Examined the synergistic effects of BH3 peptide and c-Myc in cells with varying Bax and Bak deficiencies.

    • Main Results:

    • Fibroblasts lacking Bak remained susceptible to c-Myc-induced apoptosis, while those lacking Bax were resistant.
    • c-Myc activation did not alter Bax expression, localization, or conformation.
    • Ectopic Bax expression or BH3 peptide microinjection restored c-Myc sensitivity in Bax-deficient cells.
    • BH3 peptide also restored sensitivity in p53-deficient cells, but not in cells lacking both Bax and Bak.

    Conclusions:

    • c-Myc induces apoptosis through a mechanism that requires Bax but does not involve changes in Bax expression or conformation.
    • c-Myc triggers a mitochondrial destabilizing activity that cooperates with proapoptotic Bcl-2 family members.
    • Direct activation of BH3-only domains can bypass certain resistance mechanisms to c-Myc-induced apoptosis.