Journal
CELL CYCLE
Volume 4, Issue 10, Pages 1385-1388Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.4.10.2061
Keywords
taxol; spindle checkpoint; p55CDC; Mad2; BubR1; HeLa cells
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Funding
- NCI NIH HHS [CA77263, CA39821] Funding Source: Medline
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Taxol is widely used for the treatment of human cancer. Its mechanism of action in cells is dependent on drug concentration. At low concentrations of Taxol ( 5 - 10 nM), cells exhibit aberrant mitosis, including aneuploidy, in the absence of mitotic arrest. At higher concentrations of Taxol (> 20 nM), the cell cycle is blocked at metaphase by spindle checkpoint activation. Here we demonstrate that low concentrations of Taxol cause mitotic delay, and result in an aneuploid population of cells after exit from mitosis. Low concentrations of Taxol dissociated p55CDC-Mad2 or p55CDC-BubR1 complexes after mitosis, whereas high concentrations of Taxol sustained the protein complex formation leading to mitotic block. The induction of apoptosis and aneuploidy by low concentrations of Taxol may result from chromosome missegregation caused by spindle checkpoint defects.
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