Inhibition of the ERK pathway promotes apoptosis induced by 2-chloro-2'-deoxyadenosine in the B-cell leukemia cell line EHEB

Nucleosides Nucleotides Nucleic Acids. 2006;25(9-11):1009-12. doi: 10.1080/15257770600894311.

Abstract

2-Chloro-2'-deoxyadenosine (CdA) is a nucleoside analogue active in B-cell chronic lymphocytic leukemia (B-CLL). Although the mechanism of action of CdA has been extensively investigated in leukemic cells, the possibility that this nucleoside analogue interacts with the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway has never been explored. In this study, we show that CdA, at concentrations close to the IC50, activated the ERK pathway in the B-cell line EHEB. Because activation of this pathway is assumed to exert anti-apoptotic effect, we combined CdA with inhibitors of the ERK pathway. The latter were found to enhance CdA-induced apoptosis. These results suggest that the efficacy of CdA could be strengthened by combination with inhibitors of the ERK pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Apoptosis*
  • Caspase 3 / metabolism
  • Cell Line, Tumor
  • Cladribine / pharmacology*
  • Dose-Response Relationship, Drug
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology*
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors*
  • Humans
  • Inhibitory Concentration 50
  • Lymphoma, B-Cell / drug therapy*
  • Lymphoma, B-Cell / enzymology*
  • Phosphorylation

Substances

  • Antineoplastic Agents
  • Enzyme Inhibitors
  • Cladribine
  • Extracellular Signal-Regulated MAP Kinases
  • Caspase 3