Role of prolonged mitotic checkpoint activation in the formation and treatment of cancer
Role of prolonged mitotic checkpoint activation in the formation and treatment of cancer
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DOI：
10.2217/fon.09.118
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发表时间：
2009-11-01
期刊：
影响因子：
3.3
通讯作者：
Yang, Vincent W.
中科院分区：
文献类型：
--
作者：
Dalton, W. Brian;Yang, Vincent W.
有丝分裂异常是人类癌细胞的共同特征，最近的研究提供了证据，表明这种异常可能在肿瘤发生中起致病作用，而不仅仅是偶然的作用。其中一种异常是有丝分裂检查点的长期激活，这可能是由许多驱动肿瘤形成的基因变化引起的。同时，抗有丝分裂化疗药物通过大规模诱导延长的有丝分裂检查点激活发挥其临床疗效，表明有丝分裂阻滞在人类癌症的形成和治疗中均具有影响力。然而，这种影响是如何发生的还不清楚。从这个角度来看，我们将讨论目前的证据，支持潜在的机制，延长激活的有丝分裂检查点影响肿瘤发生和抗有丝分裂化疗。
Mitotic abnormalities are a common feature of human cancer cells, and recent studies have provided evidence that such abnormalities may play a causative, rather than merely incidental role, in tumorigenesis. One such abnormality is prolonged activation of the mitotic checkpoint, which can be provoked by a number of the gene changes that drive tumor formation. At the same time, antimitotic chemotherapeutics exert their clinical efficacy through the large-scale induction of prolonged mitotic checkpoint activation, indicating that mitotic arrest is influential in both the formation and treatment of human cancer. However, how this influence occurs is not well understood. In this perspective, we will discuss the current evidence in support of the potential mechanisms by which prolonged activation of the mitotic checkpoint affects both tumorigenesis and antimitotic chemotherapy.