Antitumor activity of bortezomib alone and in combination with TRAIL in human acute myeloid leukemia

Acta Haematol. 2008;120(1):19-30. doi: 10.1159/000151511. Epub 2008 Aug 21.

Abstract

Acute myeloid leukemia (AML) is a malignant disease characterized by abnormal proliferation of clonal precursor cells. Although different strategies have been adopted to obtain complete remission, the disease actually progresses in about 60-70% of patients. Bortezomib has been used in multiple myeloma and other lymphoid malignancies because of its antitumor activity. Here we examined the sensitivity of bone marrow cells from AML patients (34 patients: 25 newly diagnosed, 4 relapsed, 5 refractory) to bortezomib alone or in combination with TRAIL, a member of the TNF family that induces apoptosis in tumor cells while sparing normal cells. Bortezomib induced cell death in blasts from each patient sample. The cytotoxic effect was dose- and time-dependent (concentration from 0.001 to 10 microM for 24 and 48 h) and was associated with a downregulation of Bcl-xL and Mcl-1, an upregulation of TRAIL-R1, TRAIL-R2, p21, activation of executioner caspases and a loss of the mitochondrial membrane potential. Moreover, low doses of bortezomib primed TRAIL-resistant AML cells for enhanced TRAIL-mediated killing. These results suggest that a combination of proteasome inhibitors and TRAIL could be effective for treating AML patients, even patients who are refractory to conventional chemotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / administration & dosage*
  • Apoptosis / drug effects
  • Boronic Acids / administration & dosage*
  • Bortezomib
  • Caspases / metabolism
  • Cell Cycle Proteins / metabolism
  • Dose-Response Relationship, Drug
  • Drug Synergism
  • Female
  • Humans
  • In Vitro Techniques
  • Leukemia, Myeloid, Acute / drug therapy*
  • Leukemia, Myeloid, Acute / metabolism
  • Leukemia, Myeloid, Acute / pathology
  • Male
  • Neoplasm Proteins / metabolism
  • Protease Inhibitors / administration & dosage*
  • Pyrazines / administration & dosage*
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • Receptors, Tumor Necrosis Factor / metabolism
  • Recombinant Proteins / administration & dosage
  • TNF-Related Apoptosis-Inducing Ligand / administration & dosage*

Substances

  • Antineoplastic Agents
  • Boronic Acids
  • Cell Cycle Proteins
  • Neoplasm Proteins
  • Protease Inhibitors
  • Pyrazines
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • Receptors, Tumor Necrosis Factor
  • Recombinant Proteins
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFRSF10A protein, human
  • TNFSF10 protein, human
  • Bortezomib
  • Caspases