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Pleiotropic effect of anticapsin on HeLa S3 cells
B Woynarowska1, A Witkowski, E Borowski
1Institute of Organic and Food Chemistry and Technology, Technical University of Gdańsk.
Acta Biochimica Polonica
|January 1, 1987
Summary
Anticapsin, an antibiotic, irreversibly inhibits HeLa S3 cell growth by primarily blocking protein synthesis. Its antiproliferative mechanism differs from tetaine, impacting nucleic acid synthesis less significantly.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Anticapsin is the terminal epoxyaminoacid moiety of tetaine.
- Tetaine exhibits antiproliferative effects on cells.
Purpose of the Study:
- To investigate the antiproliferative mechanism of anticapsin on HeLa S3 cells.
- To compare the effects of anticapsin and tetaine on cellular processes.
Main Methods:
- Assessing the impact of anticapsin on HeLa S3 cell growth.
- Measuring the incorporation of radiolabeled precursors into nucleic acids and proteins in intact and permeabilized cells.
- Evaluating the activity of DNA and RNA polymerases in cell-free systems.
Main Results:
- Anticapsin irreversibly inhibits HeLa S3 cell growth.
- It decreases the incorporation of precursors into nucleic acids and protein, with a predominant effect on protein synthesis during prolonged incubation.
- Anticapsin inhibits [3H]dTTP and [3H]UTP incorporation in permeabilized cells but does not significantly interfere with DNA or RNA polymerases in cell-free systems.
Conclusions:
- The antiproliferative mechanism of anticapsin in HeLa S3 cells is distinct from that of tetaine.
- Inhibition of protein synthesis is suggested as the primary effect of anticapsin's antiproliferative action.