Actinomycin D causes multidrug resistance and differentiation in a human rhabdomyosarcoma cell line

Cell Mol Biol (Noisy-le-grand). 1994 Mar;40(2):137-45.

Abstract

The emergence of drug-resistant tumor cells remains a major problem in cancer chemotherapy. Resistance to multiple unrelated antineoplastic drugs may be related, in part, to expression of the P-glycoprotein. The cell line RD, derived from an embryonic rhabdomyosarcoma tumor, was used as an in vitro model to examine the development of drug resistance. A cell line resistant to actinomycin D (RD-DAC) was developed by growing RD in increasing concentrations of the drug. The ID50 (concentration of drug needed to induce a 50% reduction in cell growth) of the resultant line to actinomycin D was more than 15 times that of the parental line. The resistant line was cross-resistant to vincristine and doxorubicin. Resistance to actinomycin D resulted in increased P-glycoprotein expression, which was associated with a change in desmin and vimentin expression. These results suggest that exposure to chemotherapeutic drugs can induce not only classical multidrug resistance, but also a process of cellular differentiation in rhabdomyosarcoma cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Carrier Proteins / biosynthesis
  • Cell Differentiation / drug effects*
  • Cell Division
  • DNA / analysis
  • Dactinomycin / pharmacology*
  • Desmin / metabolism
  • Drug Resistance*
  • Humans
  • Membrane Glycoproteins / biosynthesis
  • Rhabdomyosarcoma
  • Tumor Cells, Cultured
  • Vimentin / metabolism

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Carrier Proteins
  • Desmin
  • Membrane Glycoproteins
  • Vimentin
  • Dactinomycin
  • DNA