The novel receptor tyrosine kinase Axl is constitutively active in B-cell chronic lymphocytic leukemia and acts as a docking site of nonreceptor kinases: implications for therapy

Blood. 2011 Feb 10;117(6):1928-37. doi: 10.1182/blood-2010-09-305649. Epub 2010 Dec 6.

Abstract

Recently, we detected that chronic lymphocytic leukemia (CLL) B-cell-derived microvesicles in CLL plasma carry a constitutively phosphorylated novel receptor tyrosine kinase (RTK), Axl, indicating that Axl was acquired from the leukemic B cells. To examine Axl status in CLL, we determined the expression of phosphorylated-Axl (P-Axl) in freshly isolated CLL B cells by Western blot analysis. We detected differential levels of P-Axl in CLL B cells, and further analysis showed that expression of P-Axl was correlated with the other constitutively phosphorylated kinases, including Lyn, phosphoinositide-3 kinase, SyK/ζ-associated protein of 70 kDa, phospholipase C γ2 in CLL B cells. We found that these intracellular signaling molecules were complexed with P-Axl in primary CLL B cells. When Axl and Src kinases were targeted by a Src/Abl kinase inhibitor, bosutinib (SKI-606), or a specific-inhibitor of Axl (R428), robust induction of CLL B-cell apoptosis was observed in both a dose- and time-dependent manner. Therefore, we have identified a novel RTK in CLL B cells which appears to work as a docking site for multiple non-RTKs and drives leukemic cell survival signals. These findings highlight a unique target for CLL treatment.

Publication types

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

MeSH terms

  • Aniline Compounds / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Axl Receptor Tyrosine Kinase
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / enzymology
  • B-Lymphocytes / pathology
  • Benzocycloheptenes / pharmacology
  • Binding Sites
  • Coculture Techniques
  • Humans
  • Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy*
  • Leukemia, Lymphocytic, Chronic, B-Cell / enzymology*
  • Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Nitriles / pharmacology
  • Phosphorylation
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinases / metabolism
  • Proto-Oncogene Proteins / antagonists & inhibitors*
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • Quinolines / pharmacology
  • Receptor Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Stromal Cells / drug effects
  • Triazoles / pharmacology
  • src-Family Kinases / antagonists & inhibitors
  • src-Family Kinases / metabolism

Substances

  • Aniline Compounds
  • Benzocycloheptenes
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Nitriles
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Quinolines
  • Triazoles
  • bemcentinib
  • bosutinib
  • Protein Kinases
  • Receptor Protein-Tyrosine Kinases
  • src-Family Kinases
  • Axl Receptor Tyrosine Kinase
  • AXL protein, human