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Modulation of multidrug resistance in human leukemia cells with mdr1-targeted antisense oligonucleotides using

H Dassow1, D Lassner, H Remke

  • 1Department of Clinical Pharmacology, University of Leipzig, Germany.

Abstract

Insights

Antisense oligodeoxynucleotides (AS-ODNs) encapsulated with cationic lipids enhance cellular uptake and inhibit multidrug resistance (MDR) in leukemia cells. Prophylactic AS-ODN treatment shows promise for managing MDR.

Area of Science:

  • Molecular biology
  • Cancer research
  • Drug delivery systems

Background:

  • Multidrug resistance (MDR) in leukemia poses a significant challenge to effective chemotherapy.
  • The P-glycoprotein (P170) is a key mediator of MDR, contributing to drug efflux and treatment failure.
  • Antisense oligodeoxynucleotides (AS-ODNs) offer a targeted approach to downregulate genes involved in MDR, such as mdr1.

Purpose of the Study:

  • To investigate the efficacy of chimeric AS-ODNs encapsulated with cationic lipids in overcoming MDR in human leukemia cells.
  • To compare the effectiveness of lipid-conjugated AS-ODNs with traditional free AS-ODNs (unmodified or phosphorothioated).
  • To evaluate the potential of AS-ODNs for prophylactic treatment in drug-sensitive leukemia cells.

Main Methods:

  • Drug-resistant and drug-sensitive human leukemia cell lines were treated with AS-ODNs.
  • Cellular uptake of AS-ODNs was analyzed.
  • MDR-related markers, including mdr1-mRNA and P170 expression, were quantified using RT-PCR and flow cytometry (FCM).
  • Cellular accumulation and efflux of Rhodamine 123 (R123) were assessed by FCM.
  • Sensitivity to vincristine was determined using the MTT assay.

Main Results:

  • Cationic lipid encapsulation significantly increased cellular AS-ODN uptake but also introduced variability.
  • Both AS-ODN types reduced P170 expression, with chimeric AS-ODNs showing a stronger effect (30% vs. 22% reduction).
  • Inhibition of P170 expression correlated with increased sensitivity to vincristine.
  • AS-ODN treatment in drug-sensitive cells led to near-complete inhibition of mdr1-mRNA expression (5% of control).

Conclusions:

  • Complete reversal of the MDR phenotype in established drug-resistant leukemia cells using AS-ODNs is challenging.
  • Prophylactic treatment with AS-ODNs presents a more promising strategy for managing MDR in leukemia.
  • Lipid-based delivery systems enhance AS-ODN uptake and may improve therapeutic outcomes in leukemia treatment.

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