An increased tendency of genomic alterations during the life cycle of cells leads to genomic instability, which is a major driving force for tumorigenesis. A considerable fraction of tumor cells are tetraploid or aneuploid, which renders them intrinsically susceptible to mitotic aberrations, and hence, are particularly sensitive to the induction of mitotic catastrophe. Resistance to cell death is also closely linked to genomic instability, as it enables malignant cells to expand even in a stressful environment. Currently it is known that cells can die via multiple mechanisms. Mitotic catastrophe represents a step preceding apoptosis or necrosis, depending on the expression and/or proper function of several proteins. Mitotic catastrophe was proposed to be an onco-suppressive mechanism and the evasion of mitotic catastrophe constitutes one of the gateways to cancer development. Thus, stimulation of mitotic catastrophe appears to be a promising strategy in cancer treatment. Indeed, several chemotherapeutic drugs are currently used at concentrations that induce apoptosis irrespective of the cell cycle phase, yet are very efficient at triggering mitotic catastrophe at lower doses, significantly limiting side effects. In the present review we summarize current data concerning the role of mitotic catastrophe in cancer drug resistance and discuss novel strategies to break this link.

细胞生命周期中基因组改变的趋势增加，导致基因组不稳定，这是肿瘤发生的主要驱动力。肿瘤细胞的相当一部分是四倍体或非整倍体，这使得它们本质上易受有丝分裂畸变的影响，因此对诱导有丝分裂灾难特别敏感。对细胞死亡的抵抗力也与基因组不稳定性密切相关，因为它使恶性细胞即使在压力环境下也能扩增。目前已知细胞可以通过多种机制死亡。有丝分裂灾难代表了凋亡或坏死之前的一个步骤，这取决于几种蛋白质的表达和/或适当的功能。有人提出有丝分裂灾难是一种抑癌机制，而逃避有丝分裂灾难是通往癌症发展的途径之一。因此，在癌症治疗中刺激有丝分裂灾难似乎是一种有前途的策略。确实，当前使用几种化学治疗药物，其浓度可诱导凋亡，而与细胞周期阶段无关，但在较低剂量下却能非常有效地引发有丝分裂灾难，从而大大限制了副作用。在本综述中，我们总结了有关有丝分裂灾难在癌症耐药性中作用的最新数据，并讨论了打破这一联系的新策略。目前，几种化学治疗药物的使用浓度均能诱导凋亡，而与细胞周期阶段无关，但在较低剂量下却能有效触发有丝分裂灾难，从而显着限制了副作用。在本综述中，我们总结了有关有丝分裂灾难在癌症耐药性中作用的最新数据，并讨论了打破这一联系的新策略。目前，几种化学治疗药物的使用浓度均能诱导凋亡，而与细胞周期阶段无关，但在较低剂量下却能有效触发有丝分裂灾难，从而显着限制了副作用。在本综述中，我们总结了有关有丝分裂灾难在癌症耐药性中作用的最新数据，并讨论了打破这一联系的新策略。