A model for tumor cell killing by topoisomerase poisons.
Our model proposes that topoisomerase-targeting antitumor drugs form reversible drug-
enzyme-DNA complexes that collide with the DNA and RNA synthesis machineries. On
collision, the complexes lose their reversibility, and generate lethal double-strand DNA
breaks. Further investigations of topoisomerase action will allow this model to be refined,
and may ultimately lead to the development of more effective anticancer drugs.
enzyme-DNA complexes that collide with the DNA and RNA synthesis machineries. On
collision, the complexes lose their reversibility, and generate lethal double-strand DNA
breaks. Further investigations of topoisomerase action will allow this model to be refined,
and may ultimately lead to the development of more effective anticancer drugs.
Our model proposes that topoisomerase-targeting antitumor drugs form reversible drug-enzyme-DNA complexes that collide with the DNA and RNA synthesis machineries. On collision, the complexes lose their reversibility, and generate lethal double-strand DNA breaks. Further investigations of topoisomerase action will allow this model to be refined, and may ultimately lead to the development of more effective anticancer drugs.
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