Activity of selective fully human agonistic antibodies to the TRAIL death receptors TRAIL-R1 and TRAIL-R2 in primary and cultured lymphoma cells: induction of apoptosis and enhancement of doxorubicin- and bortezomib-induced cell death

Br J Haematol. 2005 Aug;130(4):501-10. doi: 10.1111/j.1365-2141.2005.05656.x.

Abstract

Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) is a death protein that preferentially kills tumour cells while sparing normal cells. TRAIL has four exclusive receptors, two of which (TRAIL-R1, TRAIL-R2) are death receptors. Both TRAIL/Apo2L and agonistic antibodies to the TRAIL death receptors are currently being explored for cancer therapy. Although the activity of TRAIL/Apo2L in a variety of haematological malignancies has been examined, the activity of anti-TRAIL receptor agonistic antibodies in primary and cultured lymphoma cells has not. Using two fully human selective agonistic monoclonal antibodies to the TRAIL death receptors TRAIL-R1 (HGS-ETR1) and TRAIL-R2 (HGS-ETR2) this study demonstrated that both monoclonal antibodies activated caspase-8 and induced cell death in five of nine human lymphoma cell lines, and induced >10% cell death in 67% and 70%, respectively, of 27 primary lymphoma cells, and >20% cell death in at least one-thirds of the samples. HGS-ETR1 and HGS-ETR2 demonstrated comparable activity in the fresh tumour samples, which was independent of TRAIL receptor surface expression, Bax, cFLIP, or procaspase-8 expression, or exposure to prior therapy. Furthermore, both antibodies enhanced the killing effect of doxorubicin and bortezomib. Our data demonstrate that HGS-ETR1 and HGS-ETR2 monoclonal antibodies can induce cell death in a variety of cultured and primary lymphoma cells, and may have therapeutic value in lymphoma.

Publication types

  • Comparative Study

MeSH terms

  • Analysis of Variance
  • Antibodies, Monoclonal / pharmacology*
  • Antineoplastic Agents / therapeutic use*
  • Apoptosis / drug effects
  • Boronic Acids / therapeutic use
  • Bortezomib
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Doxorubicin / therapeutic use
  • Drug Synergism
  • Fluorescent Antibody Technique
  • Humans
  • Lymphoma / drug therapy*
  • Lymphoma / immunology*
  • Pyrazines / therapeutic use
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • Receptors, Tumor Necrosis Factor / agonists*
  • Statistics, Nonparametric
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / immunology
  • Tumor Cells, Cultured / pathology*

Substances

  • Antibodies, Monoclonal
  • Antineoplastic Agents
  • Boronic Acids
  • Pyrazines
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • Receptors, Tumor Necrosis Factor
  • TNFRSF10A protein, human
  • TNFRSF10B protein, human
  • Bortezomib
  • Doxorubicin