Evaluation of glucocorticoid sensitivity in 697 pre-B acute lymphoblastic leukemia cells after overexpression or silencing of MAP kinase phosphatase-1

J Cancer Res Clin Oncol. 2005 Jun;131(6):347-54. doi: 10.1007/s00432-004-0659-3. Epub 2005 Mar 15.

Abstract

Purpose: To determine the effect of modulating MAP kinase phosphatase-1 (MKP-1) expression levels on cell death induced by glucocorticoid (GC) or hydroxyurea (HU) treatment in the human pre-B acute lymphoblastic leukemia cell line 697.

Methods: Stable MKP-1 overexpressing transformants of the 697 pre-B acute lymphoblastic leukemia cell line were created and tested for sensitivity to the GC triamcinolone acetonide (TA) and HU, and compared to a control 697 cell line containing normal MKP-1 expression levels. Small interfering RNAs (siRNAs) were designed to inhibit MKP-1 expression and evaluated for their effect on GC-mediated cell death.

Results: MKP-1 overexpression caused a phenotype of partial resistance to HU-induced apoptosis but not to GC-induced apoptosis. Electroporation of siRNAs effectively silenced MKP-1 expression, and increased sensitivity to TA by 9.6+/-1.9%.

Conclusions: Because MKP-1 protects certain tumor cells from chemotherapy-induced apoptosis, its inhibition is being considered as a possible strategy for combination cancer therapy. However, this study suggests that while MKP-1 inhibition may improve the efficacy of DNA damaging agents, it may have only limited utility in combination with glucocorticoids.

Publication types

  • Evaluation Study
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Base Sequence
  • Caspase 3
  • Caspases / metabolism
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism*
  • Cell Line, Tumor
  • Drug Resistance, Neoplasm
  • Dual Specificity Phosphatase 1
  • Gene Silencing*
  • Glucocorticoids / pharmacology*
  • Humans
  • Hydroxyurea / pharmacology
  • Immediate-Early Proteins / genetics
  • Immediate-Early Proteins / metabolism*
  • Immunoblotting
  • Molecular Sequence Data
  • Phosphoprotein Phosphatases / genetics
  • Phosphoprotein Phosphatases / metabolism*
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy*
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • Protein Phosphatase 1
  • Protein Tyrosine Phosphatases / genetics
  • Protein Tyrosine Phosphatases / metabolism*
  • RNA, Messenger / metabolism
  • RNA, Small Interfering / pharmacology
  • Transfection
  • Triamcinolone Acetonide / pharmacology*

Substances

  • Antineoplastic Agents
  • Cell Cycle Proteins
  • Glucocorticoids
  • Immediate-Early Proteins
  • RNA, Messenger
  • RNA, Small Interfering
  • Phosphoprotein Phosphatases
  • Protein Phosphatase 1
  • DUSP1 protein, human
  • Dual Specificity Phosphatase 1
  • Protein Tyrosine Phosphatases
  • CASP3 protein, human
  • Caspase 3
  • Caspases
  • Triamcinolone Acetonide
  • Hydroxyurea