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P-glycoprotein and multidrug resistance

M M Gottesman1, I Pastan, S V Ambudkar

  • 1Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. gottesman@od1em1.od.nih.gov

Current Opinion in Genetics & Development
|October 1, 1996
PubMed
Summary

Multidrug resistance in cancer involves P-glycoprotein, an efflux pump. This review explores its controversial mechanisms and physiological roles, clarifying its function in cancer multidrug resistance.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Multidrug resistance (MDR) in cancer is a long-standing challenge.
  • P-glycoprotein, an energy-dependent transporter, is a key mediator of MDR.
  • Despite decades of research and gene cloning, its precise mechanism and biological function remain debated.

Purpose of the Study:

  • To review current research on the mechanism of action of the multidrug transporter (P-glycoprotein).
  • To discuss proposed models, such as the hydrophobic cleaner and altered partitioning models.
  • To examine the potential function of P-glycoprotein as a chloride and/or ATP channel and the role of phosphorylation.

Main Methods:

  • Literature review of existing research on P-glycoprotein.
  • Analysis of proposed models for P-glycoprotein's mechanism of action.

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  • Synthesis of findings regarding its function, phosphorylation, and physiological role.

    • Main Results:

    • Controversy persists regarding the exact mechanism of P-glycoprotein's drug efflux.
    • P-glycoprotein may function as a chloride and/or ATP channel.
    • Phosphorylation plays a role in modulating P-glycoprotein activity.

    Conclusions:

    • The precise mechanism and physiological role of P-glycoprotein require further elucidation.
    • Understanding P-glycoprotein is crucial for overcoming cancer multidrug resistance.
    • Continued research is needed to resolve the controversies surrounding this important transporter.