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[Relation of mammalian cell resistance to actinomycin D with a change in the karyotype and a decrease in cytoplasmic
Abstract:
Djungarian hamster cell lines, selected for resistance to 2 microgram/ml of actinomycin D (AD) have been studied. These lines are 1000-4000 times more resistant to AD than the parent cells. AD-resistance is an unstable property. It is lost or diminished when the cells are grown in the absence of AD. The resistant cells show markedly reduced uptake of AD and unrelated agent - colchicin, which indicated that resistance to AD is due to the decrease of plasma membrane permeability. The chromosomal analysis of resistant lines revealed a specific abnormality in their kariotypes, namely, chromosomes containing "homogeneously staining regions" (HSR). These data support the suggestion that AD-resistance is associated with gene amplification.
Insights
Djungarian hamster cells resistant to actinomycin D (AD) showed decreased drug uptake, indicating reduced membrane permeability. This resistance was unstable and linked to chromosomal abnormalities, suggesting gene amplification.
Area of Science:
- Cell Biology
- Genetics
- Pharmacology
Context:
- Cell lines selected for resistance to actinomycin D (AD) were studied.
- Resistance levels were 1000-4000 times higher than parent cells.
Purpose:
- To investigate the mechanism of actinomycin D resistance in Djungarian hamster cells.
- To explore the relationship between drug resistance and chromosomal alterations.
Summary:
- Resistant cell lines exhibited significantly reduced uptake of AD and colchicine, suggesting decreased plasma membrane permeability.
- The acquired AD resistance was unstable, diminishing upon removal of the drug.
- Chromosomal analysis revealed homogeneously staining regions (HSR) in resistant lines, supporting a link to gene amplification.
Impact:
- Provides evidence for the role of gene amplification in conferring drug resistance.
- Highlights the potential for developing strategies to overcome drug resistance in cancer therapy.
- Contributes to understanding cellular mechanisms of multidrug resistance.