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Related Experiment Videos

BCR-ABL accelerates C2-ceramide-induced apoptosis

V Maguer-Satta1, S Burl, L Liu

  • 1The Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, Canada.

Oncogene
|February 17, 1998
PubMed
Summary

Chronic myeloid leukemia (CML) progenitor cells resist growth factor deprivation due to BCR-ABL activity. However, BCR-ABL accelerates apoptosis induced by TNF-alpha or ceramide.

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Area of Science:

  • Hematology
  • Oncology
  • Cell Biology

Background:

  • Neoplastic progenitor cells in chronic myeloid leukemia (CML) exhibit increased proliferation.
  • The resistance of these CML progenitor cells to apoptosis is a controversial topic.
  • Understanding apoptosis regulation in CML is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the apoptosis resistance of primitive CML progenitor cells.
  • To determine the role of BCR-ABL in apoptosis regulation under different conditions.
  • To compare the response of CML cells and normal progenitors to apoptosis-inducing stimuli.

Main Methods:

  • Isolation and in vitro culture of highly purified primitive CML progenitor cells and normal progenitors.
  • Assessment of cell survival and proliferation in the absence of growth factors.

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  • Induction of apoptosis using tumor necrosis factor-alpha (TNF-alpha) and ceramide.
  • Analysis of BCR-ABL signaling pathway activation during apoptosis.

    • Main Results:

    • Primitive CML progenitor cells survive and proliferate in vitro without growth factors, unlike normal progenitors.
    • Both CML and normal cells exhibit similar dose-dependent sensitivity to TNF-alpha or ceramide-induced apoptosis.
    • Ceramide treatment accelerates apoptosis in BCR-ABL+ cells, with increased phosphorylation of key signaling proteins.
    • Growth factor deprivation resistance is mediated by basal BCR-ABL activity, while ceramide enhances apoptosis via BCR-ABL kinase activation.

    Conclusions:

    • Basal BCR-ABL activity confers resistance to apoptosis under growth factor deprivation in CML progenitors.
    • BCR-ABL signaling accelerates ceramide-induced apoptosis, suggesting a dual role in apoptosis regulation.
    • These findings highlight distinct mechanisms of apoptosis control in CML and offer potential therapeutic targets.