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Perforin and granzyme B induce apoptosis in FasL-resistant colon carcinoma cells

D Vermijlen1, C J Froelich, D Luo

  • 1Laboratory for Cell Biology and Histology, Free University Brussels (VUB), Belgium. dvermijl@cyto.vub.ac.be

Cancer Immunology, Immunotherapy : CII
|July 19, 2001
PubMed

Insights

Colon carcinoma cells resist Fas ligand-induced apoptosis but are sensitive to perforin/granzyme B-induced apoptosis. This resistance occurs upstream of caspase-3 activation, indicating a specific pathway vulnerability.

Area of Science:

  • Immunology
  • Cell Biology
  • Cancer Research

Background:

  • Cytotoxic lymphocytes induce apoptosis via Fas ligand (FasL) or perforin/granzyme B pathways.
  • Fas-expressing colon carcinoma (CC) cells exhibit resistance to FasL-mediated apoptosis.

Purpose of the Study:

  • Investigate CC cell sensitivity to the perforin/granzyme B pathway.
  • Determine if FasL resistance precedes caspase-3 activation.

Main Methods:

  • Treated Fas-expressing rat CC531s cells with recombinant human soluble FasL and perforin/granzyme B.
  • Assessed apoptosis features (chromatin condensation, DNA fragmentation) and caspase-3 activity.
  • Utilized a caspase-3 inhibitor (Z-DEVD-FMK) to evaluate pathway involvement.

Main Results:

  • CC531s cells showed apoptosis features upon perforin/granzyme B treatment.
  • Caspase-3 activation occurred after perforin/granzyme B but not FasL treatment.
  • Caspase-3 inhibition blocked perforin/granzyme B-induced DNA fragmentation.

Conclusions:

  • Colon carcinoma cells are sensitive to perforin/granzyme B-induced apoptosis via caspase-3 activation.
  • FasL resistance in CC cells is located upstream of caspase-3 activation.

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