Loss of mitosis regulation is a common feature of malignant cells that leads to aberrant cell division with inaccurate chromosome segregation. The mitotic checkpoint is responsible for faithful transmission of genetic material to the progeny. Defects in this checkpoint, such as mutations and changes in gene expression, lead to abnormal chromosome content or aneuploidy that may facilitate cancer development. Furthermore, a defective checkpoint response is indicated in the development of drug resistance to microtubule poisons that are used in treatment of various blood and solid cancers for several decades. Mitotic slippage and senescence are important cell fates that occur even with an active mitotic checkpoint and are held responsible for the resistance. However, contradictory findings in both the scenarios of carcinogenesis and drug resistance have aroused questions on whether mitotic checkpoint defects are truly responsible for these dismal outcomes. Here, we discuss the possible contribution of the faulty checkpoint signaling in cancer development and drug resistance, followed by the latest research on this pathway for better outcomes in cancer treatment.

有丝分裂调节的丧失是恶性细胞的一个共同特征，它导致异常细胞分裂和不准确的染色体分离。有丝分裂检查点负责将遗传物质忠实地传递给后代。该检查点的缺陷，例如基因表达的突变和变化，会导致染色体含量异常或非整倍体，从而可能促进癌症的发展。此外，几十年来用于治疗各种血液和实体癌的微管毒物的耐药性发展表明检查点反应有缺陷。有丝分裂滑移和衰老是重要的细胞命运，即使在有丝分裂检查点活跃的情况下也会发生，并且对抵抗负责。然而，在致癌作用和耐药性两种情况下的矛盾发现引发了关于有丝分裂检查点缺陷是否真正导致这些令人沮丧的结果的问题。在这里，我们讨论了错误的检查点信号在癌症发展和耐药性中的可能贡献，然后是关于该途径的最新研究，以便在癌症治疗中获得更好的结果。