Regulation of PTEN by CK2 and Notch1 in primary T-cell acute lymphoblastic leukemia: rationale for combined use of CK2- and gamma-secretase inhibitors

Haematologica. 2010 Apr;95(4):674-8. doi: 10.3324/haematol.2009.011999. Epub 2009 Dec 16.

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) patients frequently display NOTCH1 activating mutations and Notch can transcriptionally down-regulate the tumor suppressor PTEN. However, it is not clear whether NOTCH1 mutations associate with decreased PTEN expression in primary T-ALL. Here, we compared patients with or without NOTCH1 mutations and report that the former presented higher MYC transcript levels and decreased PTEN mRNA expression. We recently showed that T-ALL cells frequently display CK2-mediated PTEN phosphorylation, resulting in PTEN protein stabilization and concomitant functional inactivation. Accordingly, the T-ALL samples analyzed, irrespectively of their NOTCH1 mutational status, expressed significantly higher PTEN protein levels than normal controls. To evaluate the integrated functional impact of Notch transcriptional and CK2 post-translational inactivation of PTEN, we treated T-ALL cells with both the gamma-secretase inhibitor DAPT and the CK2 inhibitors DRB/TBB. Our data suggest that combined use of gamma-secretase and CK2 inhibitors may have therapeutic potential in T-ALL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid Precursor Protein Secretases / antagonists & inhibitors*
  • Amyloid Precursor Protein Secretases / metabolism
  • Blotting, Western
  • Casein Kinase II / antagonists & inhibitors*
  • Casein Kinase II / metabolism*
  • Cell Proliferation / drug effects
  • Cell Size / drug effects
  • Child
  • Dichlororibofuranosylbenzimidazole / pharmacology
  • Drug Therapy, Combination
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation, Leukemic
  • Humans
  • Mutation / genetics
  • PTEN Phosphohydrolase / genetics*
  • PTEN Phosphohydrolase / metabolism
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptor, Notch1 / genetics*
  • Receptor, Notch1 / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Triazoles / pharmacology

Substances

  • 4,5,6,7-tetrabromobenzotriazole
  • Enzyme Inhibitors
  • NOTCH1 protein, human
  • RNA, Messenger
  • Receptor, Notch1
  • Triazoles
  • Dichlororibofuranosylbenzimidazole
  • Casein Kinase II
  • PTEN Phosphohydrolase
  • PTEN protein, human
  • Amyloid Precursor Protein Secretases