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Related Experiment Videos

Multiple pathways of TWEAK-induced cell death.

Masafumi Nakayama1, Kazumi Ishidoh, Nobuhiko Kayagaki

  • 1Department of Immunology, Allergy Research Center, Division of Pathology, Central Laboratory of Medical Sciences, Juntendo University School of Medicine, Tokyo, Japan.

Journal of Immunology (Baltimore, Md. : 1950)
|January 5, 2002
PubMed
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Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) triggers distinct cell death pathways, including apoptosis and necrosis, depending on the cell type. TWEAK utilizes receptors other than DR3, indicating diverse mechanisms of action in cancer cells.

Area of Science:

  • Immunology
  • Cell Biology
  • Cancer Research

Background:

  • Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a cytokine involved in inflammation and cell death.
  • TWEAK belongs to the TNF superfamily and is expressed on IFN-gamma-stimulated monocytes.
  • Its role in inducing cell death in various tumor cell lines requires detailed characterization.

Purpose of the Study:

  • To investigate the distinct mechanisms of TWEAK-induced cell death in different tumor cell lines.
  • To identify the specific pathways and receptors involved in TWEAK-mediated apoptosis and necrosis.
  • To elucidate the cell type-specific responses to TWEAK stimulation.

Main Methods:

  • Characterization of TWEAK-induced cell death in Kym-1, HSC3, and IFN-gamma-treated HT-29 cells.

Related Experiment Videos

  • Assessment of the roles of TNF-alpha, cycloheximide, and specific inhibitors (caspase and lysosomal proteinase inhibitors) in TWEAK-induced cell death.
  • Analysis of TWEAK receptor expression (DR3) and binding (CD8-TWEAK) on sensitive tumor cell lines.
  • Detection of caspase activation and cathepsin B release.

    • Main Results:

    • TWEAK induced TNF-alpha-mediated cell death in Kym-1 cells, inhibited by cycloheximide.
    • TWEAK triggered direct cell death in HSC3 and IFN-gamma-treated HT-29 cells, independent of TNF-alpha and cycloheximide.
    • HSC3 cells underwent caspase-dependent apoptosis, while HT-29 cells exhibited cathepsin B-dependent necrosis.
    • TWEAK-sensitive cells did not express DR3 but specifically bound CD8-TWEAK, suggesting alternative TWEAK receptors.

    Conclusions:

    • TWEAK induces multiple cell death pathways, including caspase-dependent apoptosis and cathepsin B-dependent necrosis.
    • The mode of TWEAK-induced cell death is cell type-specific.
    • TWEAK mediates its effects through receptors distinct from DR3.