Phenotypic reversion of cisplatin resistance in human cells accompanies reduced host cell reactivation of damaged plasmid.

Chuck C.-K. Chao, YL Lee, S Lin-Chao

Research output: Contribution to journalJournal Article peer-review

Abstract

Revertant cell lines were established from cisplatin (CP) resistant HeLa cells. Expression of CP damaged plasmid DNA carrying bacterial chloramphenicol acetyltransferase (CAT) gene after transfection into cells was measured. Revertant cells showed reduced host cell reactivation of damaged plasmid, as compared to resistant cells. Addition of aphidicolin, an inhibitor for DNA polymerase alpha, to resistant cells effectively blocked enhanced plasmid reactivation and acquired resistance. The results are consistent with the notion that cellular ability in repair CP-damaged DNA is a mechanism for CP resistance.
Original languageAmerican English
Pages (from-to)851-859
JournalBiochemical and Biophysical Research Communications
Volume170
Issue number2
DOIs
StatePublished - 1990

Keywords

  • Aphidicolin
  • Cell Survival
  • Cisplatin/administration & dosage
  • Cisplatin/pharmacology
  • DNA Damage
  • DNA Repair
  • DNA/drug effects
  • Diterpenes/pharmacology
  • Dose-Response Relationship, Drug
  • Drug Resistance
  • HeLa Cells
  • Humans
  • Phenotype
  • Plasmids/drug effects

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