Estramustine depolymerizes microtubules by binding to tubulin

摘要: Abstract To investigate the mechanism of action antineoplastic drug estramustine, we compared its effects on human prostate cancer cells with those vinblastine. At their respective concentrations that result in 50% inhibition clonogenic growth, both drugs caused an accumulation blocked at mitosis and similar dose- time-dependent depolymerization interphase microtubules. Also, colcemid-resistant colcemid-hypersensitive Chinese hamster ovary tubulin mutations were collaterally cross-resistant or -sensitive to estramustine. Thus, cytotoxicity estramustine is due microtubule properties. This could be by interaction and/or microtubule-associated proteins (MAPs). Previous investigations have shown high phosphate can inhibit polymerization vitro binding MAPs. However, clinical prodrug intracellular active compound. In this study, investigated MAPs taxol-stabilized microtubulesin vivo. contrast previous reports, no effect microtubules was found. Furthermore, found purified inhibited vitro. Taken together, these results demonstrate causes direct tubulin. The costs publication article defrayed part payment page charges. must therefore hereby marked advertisement accordance 18 U.S.C. Section 1734 solely indicate fact.