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2-deoxy-D-glucose toxicity and transport in human multidrug-resistant KB carcinoma cell lines

J Bentley1, S E Bell, D M Quinn

  • 1Department of Biology, The University of York, UK.

Oncology Research
|January 1, 1996
PubMed

Insights

Multidrug-resistant (MDR) cancer cells show increased sensitivity to 2-deoxy-D-glucose, linked to reduced levels of the GLUT-1 glucose transporter. This suggests GLUT-1 alterations are key in MDR cell responses.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Pharmacology

Background:

  • Multidrug resistance (MDR) is a major challenge in cancer chemotherapy.
  • Colateral sensitivity, where resistant cells become sensitive to other drugs, is an emerging therapeutic concept.
  • 2-deoxy-D-glucose (2-DG) is a glucose analog that can be used to study glucose metabolism.

Purpose of the Study:

  • To investigate the relationship between multidrug resistance and collateral sensitivity to 2-deoxy-D-glucose in human KB carcinoma cell lines.
  • To elucidate the role of the GLUT-1 glucose transporter in this observed collateral sensitivity.

Main Methods:

  • Development of colchicine-selected multidrug-resistant (MDR) human KB carcinoma cell lines.
  • Assessment of 2-deoxy-D-glucose resistance and accumulation in parental and MDR cell lines.
  • Analysis of 2-deoxy-D-glucose uptake kinetics.
  • Quantification of GLUT-1 transporter levels using Western blot analysis.

Main Results:

  • MDR cell lines exhibited increasing collateral sensitivity to 2-deoxy-D-glucose, correlating with increased drug resistance.
  • 2-deoxy-D-glucose accumulation and uptake were reduced in MDR cells, inversely correlating with collateral sensitivity.
  • Significantly reduced levels of the GLUT-1 facilitative transporter were observed in MDR cell lines, correlating with 2-DG toxicity and uptake.

Conclusions:

  • The response of human KB MDR cells to 2-deoxy-D-glucose is associated with alterations in the level and activity of the GLUT-1 glucose transporter.
  • Reduced GLUT-1 expression and function contribute to the collateral sensitivity observed in multidrug-resistant cancer cells.

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