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首页> 外文期刊>Cell cycle >Low concentrations of taxol cause mitotic delay followed by premature dissociation of p55CDC from Mad2 and BubR1 and abrogation of the spindle checkpoint, leading to aneuploidy.
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Low concentrations of taxol cause mitotic delay followed by premature dissociation of p55CDC from Mad2 and BubR1 and abrogation of the spindle checkpoint, leading to aneuploidy.

机译：低浓度的紫杉醇引起有丝分裂延迟，随后p55CDC从Mad2和BubR1过早解离，纺锤体检查点消失，导致非整倍性。

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摘要

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.
机译：紫杉酚被广泛用于治疗人类癌症。它在细胞中的作用机制取决于药物浓度。在低浓度的紫杉醇（5-10 nM）下，细胞在不存在有丝分裂停滞的情况下会出现异常的有丝分裂，包括非整倍性。在较高的紫杉酚浓度（> 20 nM）下，细胞周期在中期被纺锤体检查点激活所阻断。在这里，我们证明低浓度的紫杉酚会导致有丝分裂延迟，并导致有丝分裂退出后细胞呈非整倍体。有丝分裂后低浓度的紫杉醇解离了p55CDC-Mad2或p55CDC-BubR1复合物，而高浓度的紫杉醇则维持了蛋白质复合物的形成，导致有丝分裂阻滞。低浓度紫杉醇诱导细胞凋亡和非整倍性可能是由纺锤体检查点缺陷引起的染色体错聚引起的。

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