Do cMOAT (MRP2), other MRP homologues, and LRP play a role in MDR?

Seminars in Cancer Biology
P BorstR Evers

Abstract

The discovery of the Multidrug Resistance-associated Protein (MRP or MRP1) as a GS-X pump able to transport both anionic drug conjugates and unmodified anti-cancer drugs out of the cell, has raised the question whether other members of the MRP family might contribute to drug resistance of human tumours. The most extensively studied member of this family is cMOAT, the canalicular Multispecific Organic Anion Transporter. The substrate specificity of this pump was originally defined by an inborn error in rats, lacking this protein. These rats are mildly hyperbilirubinemic, because of their inability to secrete bilirubin glucuronides into their bile. In addition, they have diminished capacity to secrete a variety of other organic anions. Absence of cMOAT in humans results in an analogous inborn error of metabolism, the Dubin-Johnson syndrome. Attempts to determine the effect of cMOAT on the sensitivity of cells to anti-cancer drugs have run into technical problems. Most cells transfected with a cMOAT cDNA construct and overproducing cMOAT seem unable to transport the protein to the cell surface and are not MDR. However, in polarized kidney cell monolayers cMOAT is correctly routed to the apical cell surface and able to transport vi...Continue Reading

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