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The multidrug resistance phenotype: 31P nuclear magnetic resonance characterization and 2-deoxyglucose toxicity

O Kaplan1, J W Jaroszewski, R Clarke

  • 1Medicine Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892.

Cancer Research
|March 15, 1991
PubMed

Insights

31P nuclear magnetic resonance (NMR) reveals distinct metabolic shifts in multidrug-resistant (MDR) cancer cells, including higher ATP and phosphocreatine levels. These biochemical changes, identified via NMR, correlate with increased toxicity of 2-deoxyglucose in resistant cell lines.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Medical Physics

Background:

  • Multiple drug resistance (MDR) is a major challenge in cancer chemotherapy.
  • Understanding the biochemical underpinnings of MDR is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate biochemical alterations associated with MDR using 31P nuclear magnetic resonance (NMR) spectroscopy.
  • To explore the relationship between MDR, cellular metabolism, and the toxicity of 2-deoxyglucose.

Main Methods:

  • Studied 31P NMR spectra of various wild-type and drug-resistant cancer cell lines, including those selected with Adriamycin and transfected with the MDR1 gene.
  • Assessed the toxicity of 2-deoxyglucose in sensitive and resistant cell lines.

Main Results:

  • 31P NMR spectra of resistant cells differed significantly from sensitive cells, showing increased cytoplasmic ATP and phosphocreatine levels.
  • Observed notable changes in glycerophosphocholine and glycerophosphoethanolamine levels.
  • Multidrug-resistant cells exhibited consistently higher toxicity to 2-deoxyglucose, with MCF-7 cells showing increased toxicity correlating with resistance levels.

Conclusions:

  • 31P NMR is a suitable technique for studying biochemical changes in MDR.
  • Metabolic alterations in MDR are complex and influenced by the selection drug, not solely by P-glycoprotein expression.
  • Increased 2-deoxyglucose toxicity in MDR cells suggests metabolic vulnerabilities exploitable for therapy.

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