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Related Experiment Videos

Myc-mediated apoptosis

Y Kuchino1, A Asai, C Kitanaka

  • 1Biophysics Division, National Cancer Research Institute, Tokyo, Japan.

Progress in Molecular and Subcellular Biology
|January 1, 1996
PubMed
Summary

The intron-less s-Myc gene suppresses glioma cell growth and tumorigenicity. Overexpression of s-Myc induces apoptosis in glioma cells, distinct from c-Myc.

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MEK-ERK-dependent multiple caspase activation by mitochondrial proapoptotic Bcl-2 family proteins is essential for heavy ion irradiation-induced glioma cell death.

Cell death & disease·2011

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Mammalian cells possess intron-less myc genes, including rat s-myc and human myc L2.
  • These genes are specifically expressed in tissues like rat embryo chondrocytes and human testis.

Purpose of the Study:

  • To investigate the role of s-Myc in regulating glioma cell growth and tumorigenicity.
  • To determine if s-Myc overexpression induces apoptosis in glioma cells and compare it to c-Myc.

Main Methods:

  • Analysis of s-Myc expression in glioma cells.
  • Assessment of glioma cell growth activity and tumorigenicity following s-Myc manipulation.
  • Induction and observation of apoptotic cell death in glioma cells upon s-Myc overexpression.

Main Results:

  • s-Myc expression was found to suppress the growth activity and tumorigenicity of glioma cells.
  • s-Myc functions as a negative regulator in tumor growth.
  • Overexpression of s-Myc effectively induced apoptotic cell death in human and rat glioma cells, even without serum deprivation.

Conclusions:

  • s-Myc acts as a tumor suppressor in glioma.
  • The apoptotic mechanism induced by s-Myc is distinct from that mediated by c-Myc.
  • s-Myc represents a potential therapeutic target for glioma treatment.

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