Multidrug resistance mediated by P-glycoproteins

Semin Cancer Biol. 1991 Aug;2(4):213-26.

Abstract

Overexpression of P-glycoprotein genes is a well-established cause of one form of multidrug resistance. P-glycoproteins are plasma membrane proteins containing two ATP-binding sites and twelve putative transmembrane segments. P-glycoproteins are thought to act as ATP-dependent drug efflux pumps, actively extruding a range of structurally different, hydrophobic drugs from the cell. This simple model can account for the properties of multidrug resistant cells, even those that seem to require more complex explanations. The structure and function of P-glycoprotein genes has been studied in mammals and in several lower eukaryotes. These studies are helping to delineate the range of drugs that can be transported by P-glycoproteins; the genetic mechanisms that can lead to elevated cellular P-glycoproteins levels; and the evolution of the versatile and prolific P-glycoprotein gene family. The physiological function of the human P-glycoproteins encoded by the MDR1 and MDR3 (or MDR2) genes remains a matter of speculation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Animals
  • Antineoplastic Agents / pharmacokinetics
  • Antineoplastic Agents / pharmacology
  • Chromosome Mapping
  • Cricetinae
  • Drug Resistance / genetics
  • Drug Resistance / physiology*
  • Humans
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / physiology*
  • Mice

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Antineoplastic Agents
  • Membrane Glycoproteins