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[Cellular resistance to DNA-topoisomerase II inhibitors]

A Jacquemin-Sablon1, K Bojanowski, M R Casabianca-Pignède

  • 1CNRS URA147-INSERM U140, unité de biochimie et enzymologie, institut Gustave-Roussy, Villejuif, France.

Bulletin Du Cancer
|May 1, 1994
PubMed

Insights

Chinese hamster lung cells resistant to 9-OH-ellipticine exhibit multidrug resistance (MDR). This resistance is linked to decreased topoisomerase II beta and P-glycoprotein 1 (pgp1) overexpression, with myc oncogene influencing pgp3 expression.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Context:

  • Chinese hamster lung cells (DC-3F/9-OH-E) display significant resistance (150-fold) to 9-OH-ellipticine.
  • These cells exhibit cross-resistance to various topoisomerase II (topo-II) inhibitors and natural product chemotherapeutics, indicating a complex multidrug-resistant (MDR) phenotype.

Purpose:

  • To investigate the molecular mechanisms underlying the complex drug resistance phenotype in DC-3F/9-OH-E cells.
  • To analyze the expression levels of topoisomerase II alpha and beta, and P-glycoprotein genes in relation to drug resistance.

Summary:

  • The resistant cells show a marked decrease in topoisomerase II beta and a reduction in topoisomerase II alpha. The MDR phenotype is attributed to the overexpression of the pgp1 gene.
  • Expression of pgp3 is positively regulated by the myc oncogene; myc overexpression leads to pgp3 overexpression and reversal of the MDR phenotype.

Impact:

  • This study elucidates the intricate interplay between topoisomerase II isoforms, P-glycoprotein expression, and oncogene regulation in conferring multidrug resistance.
  • Understanding these mechanisms can inform the development of novel therapeutic strategies to overcome drug resistance in cancer treatment.

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