Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic

Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14907-12. doi: 10.1073/pnas.0606176103. Epub 2006 Sep 22.

Abstract

Cell killing is a critical pharmacological activity of imatinib to eradicate Bcr/Abl+ leukemias. We found that imatinib kills Bcr/Abl+ leukemic cells by triggering the Bcl-2-regulated apoptotic pathway. Imatinib activated several proapoptotic BH3-only proteins: bim and bmf transcription was increased, and both Bim and Bad were activated posttranslationally. Studies using RNAi and cells from gene-targeted mice revealed that Bim plays a major role in imatinib-induced apoptosis of Bcr/Abl+ leukemic cells and that the combined loss of Bim and Bad abrogates this killing. Loss of Bmf or Puma had no effect. Resistance to imatinib caused by Bcl-2 overexpression or loss of Bim (plus Bad) could be overcome by cotreatment with the BH3 mimetic ABT-737. These results demonstrate that Bim and Bad account for most, perhaps all, imatinib-induced killing of Bcr/Abl+ leukemic cells and suggest previously undescribed drug combination strategies for cancer therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism*
  • Bcl-2-Like Protein 11
  • Benzamides
  • Biphenyl Compounds / pharmacology*
  • Cell Line, Tumor
  • Cell Transformation, Neoplastic
  • Cytotoxicity, Immunologic / drug effects*
  • Drug Resistance, Neoplasm*
  • Fetus / cytology
  • Fusion Proteins, bcr-abl
  • Humans
  • Imatinib Mesylate
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Liver / cytology
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Myeloid Progenitor Cells / cytology
  • Nitrophenols
  • Piperazines / pharmacology*
  • Protein-Tyrosine Kinases / metabolism*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Pyrimidines / pharmacology*
  • Sulfonamides
  • bcl-Associated Death Protein / metabolism*

Substances

  • ABT-737
  • Antineoplastic Agents
  • Apoptosis Regulatory Proteins
  • BCL2L11 protein, human
  • Bcl-2-Like Protein 11
  • Bcl2l11 protein, mouse
  • Benzamides
  • Biphenyl Compounds
  • Membrane Proteins
  • Nitrophenols
  • Piperazines
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Pyrimidines
  • Sulfonamides
  • bcl-Associated Death Protein
  • Imatinib Mesylate
  • Protein-Tyrosine Kinases
  • Fusion Proteins, bcr-abl