The spindle assembly checkpoint (SAC) is a surveillance mechanism that prevents unequal segregation of chromosomes during mitosis. Abnormalities in the SAC are associated with chromosome instability and resultant aneuploidy. This study was performed to evaluate the SAC competence in canine malignant melanoma (CMM) using four aneuploid cell lines (CMeC1, CMeC2, KMeC, and LMeC). After treatment with nocodazole, a microtubule disrupting agent, CMeC1, KMeC, and LMeC cells were arrested in M phase, whereas CMeC2 cells were not arrested, and progressed into the next cell cycle phase without cytokinesis. Chromosome spread analysis revealed a significantly increased rate of premature sister chromatid separation in CMeC2 cells. Expression of the phosphorylated form of the SAC regulator, monopolar spindle 1 (Mps1), was lower in CMeC2 cells than in the other CMM cell lines. These results indicate that the SAC is defective in CMeC2 cells, which may partially explain aneuploidy in CMM. Thus, CMeC2 cells may be useful for further studies of the SAC mechanism in CMM and in determining the relationship between SAC incompetence and aneuploidy.

纺锤体组装检查点 (SAC) 是一种监视机制，可防止有丝分裂期间染色体的不均等分离。SAC 中的异常与染色体不稳定和由此产生的非整倍体有关。本研究使用四种非整倍体细胞系（CMeC1、CMeC2、KMeC 和 LMeC）评估犬恶性黑色素瘤 (CMM) 的 SAC 能力。用诺考达唑处理后，微管破坏剂 CMeC1、KMeC 和 LMeC 细胞在 M 期停滞，而 CMeC2 细胞没有停滞，并在没有胞质分裂的情况下进入下一个细胞周期阶段。染色体扩散分析显示 CMeC2 细胞中早产姐妹染色单体分离率显着增加。SAC 调节剂的磷酸化形式的表达，单极纺锤体 1 (Mps1)，在 CMeC2 细胞中低于其他 CMM 细胞系。这些结果表明 CMeC2 细胞中的 SAC 有缺陷，这可能部分解释了 CMM 中的非整倍性。因此，CMeC2 细胞可能有助于进一步研究 CMM 中的 SAC 机制以及确定 SAC 无能与非整倍体之间的关系。