Reversal of breast cancer resistance protein-mediated drug resistance by tryprostatin A

Int J Cancer. 2003 Dec 10;107(5):721-8. doi: 10.1002/ijc.11444.

Abstract

MDR in human cancers is one of the major causes of failure of chemotherapy. A member of the superfamily of ABC transporters, BCRP, was demonstrated to confer an atypical MDR phenotype to tumor cells. To overcome the BCRP-mediated drug resistance, the fungal secondary metabolite TPS-A, a diketopiperazine, was analyzed with regard to its potency to reverse the BCRP-mediated drug-resistant phenotype. At concentrations of 10-50 microM, TPS-A reversed a mitoxantrone-resistant phenotype and inhibited the cellular BCRP-dependent mitoxantrone accumulation in the human gastric carcinoma cell line EPG85-257RNOV, the human breast cancer cell line MCF7/AdrVp (both exhibiting acquired BCRP-mediated MDR) and the BCRP cDNA-transfected breast cancer cell line MCF-7/BCRP clone 8. No cytotoxicity was seen at effective concentrations. These data indicate that TPS-A is a novel BCRP inhibitor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acridines / pharmacology*
  • Antineoplastic Agents / toxicity*
  • Breast Neoplasms / pathology*
  • Cell Division / drug effects
  • Daunorubicin / toxicity
  • Drug Resistance, Multiple / drug effects*
  • Female
  • Humans
  • Indole Alkaloids / pharmacology*
  • Kinetics
  • Mitoxantrone / toxicity
  • Piperazines / pharmacology*
  • Stomach Neoplasms
  • Tetrahydroisoquinolines / pharmacology*
  • Tumor Cells, Cultured

Substances

  • Acridines
  • Antineoplastic Agents
  • Indole Alkaloids
  • Piperazines
  • Tetrahydroisoquinolines
  • tryprostatin A
  • Mitoxantrone
  • Elacridar
  • Daunorubicin