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Related Experiment Videos

Tumor cell membrane as a potential target for methyl-beta-cyclodextrin

P Y Grosse1, F Bressolle, P Vago

  • 1Department of Oncological Pharmacology, Val d'Aurelle Anticancer Center, Parc Euromedecine, Montpellier, France.

Anticancer Research
|May 6, 1998
PubMed
Summary

Methyl-beta-cyclodextrin (MEBCD) enhances doxorubicin (DOX) accumulation in multidrug-resistant cancer cells more effectively than verapamil. MEBCD also alters cell membranes but does not affect cell cycle distribution.

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Area of Science:

  • Pharmacology
  • Cancer Biology
  • Drug Delivery

Background:

  • Multidrug resistance (MDR) is a major challenge in cancer chemotherapy, limiting the efficacy of drugs like doxorubicin (DOX).
  • Cyclodextrins, particularly methyl-beta-cyclodextrin (MEBCD), are explored for their potential to modulate drug-cell interactions and overcome resistance mechanisms.

Purpose of the Study:

  • To investigate the role of methyl-beta-cyclodextrin (MEBCD) in combination with doxorubicin (DOX) on intracellular DOX accumulation and efflux.
  • To compare the efficacy of MEBCD with verapamil, a known MDR modulator, in sensitive (HL-60 S) and multidrug-resistant (HL-60 R) human cancer cell lines.
  • To examine the effects of MEBCD on cancer cell membrane integrity and morphology.

Main Methods:

  • Utilized HL-60 S and HL-60 R human cancer cell lines.

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  • Administered methyl-beta-cyclodextrin (MEBCD) in combination with doxorubicin (DOX) at a concentration of 10 μmol per 10^6 cells.
  • Quantified intracellular DOX accumulation and efflux over the exposure period.
  • Assessed cell membrane and nuclear modifications induced by MEBCD.
  • Compared MEBCD's effects with verapamil.

    • Main Results:

    • MEBCD significantly enhanced intracellular DOX concentration in both HL-60 S and HL-60 R cell lines.
    • In the resistant HL-60 R subline, MEBCD demonstrated higher efficacy in enhancing DOX accumulation compared to verapamil.
    • MEBCD treatment led to modifications in cell membrane integrity and morphology.
    • MEBCD did not influence the distribution of cells within the cell cycle.

    Conclusions:

    • Methyl-beta-cyclodextrin (MEBCD) is effective in increasing intracellular doxorubicin (DOX) levels in both sensitive and multidrug-resistant cancer cells.
    • MEBCD shows superior activity over verapamil in overcoming doxorubicin resistance in HL-60 R cells.
    • MEBCD induces changes in cancer cell membranes, suggesting a potential mechanism for enhancing drug uptake, without impacting cell cycle progression.