Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells

Hematology. 2011 Mar;16(2):95-9. doi: 10.1179/102453311X12902908412039.

Abstract

Imatinib is a chemotherapeutic drug used for the treatment of chronic myeloid leukemia (CML). Recent data showed imatinib-induced cell death in various types of cancers. Autophagy is the physiological process in which cellular components are broken down by the lysosomal activation. In this study, we aimed to examine the effects of imatinib on autophagy in addition to apoptosis in CML cells. Results suggested that imatinib induces autophagy in CML cells through inducing over-expression of BECLIN-1 and ATG5 genes with the statistical significance. Our results demonstrated that autophagy might be involved in imatinib-induced cell death.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis Regulatory Proteins / drug effects*
  • Autophagy / drug effects*
  • Autophagy / genetics
  • Autophagy-Related Protein 5
  • Beclin-1
  • Benzamides
  • Cell Line, Tumor
  • Humans
  • Imatinib Mesylate
  • Immunoblotting
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism*
  • Membrane Proteins / drug effects*
  • Microtubule-Associated Proteins / drug effects*
  • Piperazines / pharmacology*
  • Piperazines / therapeutic use
  • Pyrimidines / pharmacology*
  • Pyrimidines / therapeutic use
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • ATG5 protein, human
  • Antineoplastic Agents
  • Apoptosis Regulatory Proteins
  • Autophagy-Related Protein 5
  • BECN1 protein, human
  • Beclin-1
  • Benzamides
  • Membrane Proteins
  • Microtubule-Associated Proteins
  • Piperazines
  • Pyrimidines
  • Imatinib Mesylate