Li Shuang,Tan Bin,Liu Xueqing,Chen Xuemei,Ding Yubin,Yu Qiubo,Chen Qian,Wang Yingxiong,He Junlin.Effect of kinetochore variation on chromosomal instability in SW626 cells[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(07):667-670.
Li Shuang,Tan Bin,Liu Xueqing,Chen Xuemei,Ding Yubin,Yu Qiubo,Chen Qian,Wang Yingxiong,He Junlin.Effect of kinetochore variation on chromosomal instability in SW626 cells[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(07):667-670.DOI：
目的 探讨恶性肿瘤细胞染色体不稳定性的可能机制。 方法 采用本实验室建立的kinetochore-NOR同步银染技术，对SW626细胞染色体kinetochore变异进行分析。 结果 与正常人外周血细胞相比，SW626细胞染色体kinetochore缺失[132(0.89%) vs 26(0.18%)]、kinetochore迟滞复制[82(0.55%) vs 14(0.10%)]和kinetochore-NOR融合[153(1.03%) vs 51(0.37%)]频率显著升高（P0.01），而不对称kinetochore频率二者差异性不显著（P0.05）。此外，在某些SW626细胞染色体上还观察到多重kinetochores现象。 结论 kinetochore 缺失、kinetochore迟滞复制和kinetochore-NOR融合可能是SW626细胞染色体非整倍性变异起源的诱因之一；染色体多重kinetochores可能是恶性肿瘤细胞染色体结构畸变产生的重要途径之一。
Abstract
Objective To probe possible mechanism of chromosomal instability in tumor. Methods Kinetochore variation was analyzed by an improved method for staining kinetochores of human chromosomes in SW626 cells. Results Compared to normal cells
the frequency of kinetochore loss[132(0.89%) vs 26(0.18%)]
kinetochore duplication laggard [82(0.55%) vs 14(0.10%)] and kinetochore-NOR fusion [153(1.03%) vs 51(0.37%)] in SW626 cells was significantly higher than those of human normal periphoreal blood cells respectively（P0.01）. Kinetochore dissymmetry had no significant difference between SW626 cells and normal control cells（P0.05）. A cyto-genentic phenomenon of multi-kinetochores was observed in SW626 cells. Conclusion Kinetochore loss
duplication laggard and kinetochore-NOR fusion might be potential origin of aneuploidy production
and multikineto-chores might be a new mechanism for inducing chromosomal structure abnormality in tumor cells.
京公网安备11010802024621