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Related Experiment Videos

TWEAKing death.

Jonathan D Ashwell1

  • 1Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. jda@pop.nci.nih.gov

The Journal of Cell Biology
|July 9, 2008
PubMed
Summary
This summary is machine-generated.

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Smac mimetics and the cytokine TWEAK induce tumor cell death through similar pathways. Both reduce levels of cellular inhibitor of apoptosis proteins (cIAP1/2), offering potential for cancer therapy.

Area of Science:

  • Cellular biology
  • Molecular oncology
  • Immunology

Background:

  • Smac mimetics induce tumor cell death by degrading cellular inhibitor of apoptosis proteins (cIAP1/2), activating NF-κB and TNF signaling.
  • Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a cytokine involved in cell death pathways.

Purpose of the Study:

  • To investigate the similarities between TWEAK-induced and Smac mimetic-induced tumor cell death.
  • To explore the role of cIAP1/2 degradation in these pathways.

Main Methods:

  • Comparative analysis of cell death signaling pathways.
  • Assessment of protein degradation and activation markers.

Main Results:

  • TWEAK and Smac mimetics trigger tumor cell death through remarkably similar events.

Related Experiment Videos

  • A common, necessary feature is the reduction of cIAP1 and, in some cases, cIAP2 and TNF receptor-associated factor 2.
  • These similarities are also observed in TNF receptor 2 signaling.

    • Conclusions:

    • Cell death pathways induced by TWEAK and Smac mimetics share common regulatory mechanisms involving cIAP1/2.
    • Induced cIAP deficiency (cIDE) may be a viable strategy for selective elimination of neoplastic cells.