论文部分内容阅读
染色体非整倍性畸变是恶性肿瘤细胞的显著细胞遗传学特征,但其诱发染色体数目不稳定的机制一直尚未阐明。本研究从与染色体分离直接相关的动粒(kinetochore)角度,采用kine-tochore-NOR同步银染技术对HEP-2细胞染色体kinetochore变异进行分析,以探讨恶性肿瘤细胞染色体数目变异的形成机制。实验共分析HEP-2细胞分裂相308个,计染色体16 962条,正常对照个体外周血细胞分裂相300个,计染色体13 800条。结果表明:与正常人外周血细胞相比,HEP-2细胞染色体kinetochore缺失和kinetochore迟滞复制频率显著升高(P<0.01),而kinetochore-NOR融合频率二者没有显著差异(P>0.05),这些结果提示kinetochore缺失和kinetochore迟滞复制可能是HEP-2细胞染色体非整倍性变异起源的诱因之一。此外,我们还在某些HEP-2细胞染色体上观察到多重kinetochore现象,并认为染色体多重kinetochore可能是恶性肿瘤细胞染色体结构畸变产生的一个新的途径。
Chromosome aneuploidy aberration is a significant cytogenetic feature of malignant tumor cells, but the mechanism of its instability induced chromosome number has not yet been elucidated. In this study, kinetic tochore-NOR synchronous silver staining was used to analyze the kinetochore variation in HEP-2 cells from the point of view of kinetochore, which is directly related to chromosome segregation, to investigate the mechanism of chromosome number variation in malignant tumor cells. A total of 308 HEP-2 cell divisions were analyzed in the experiment, accounting for 16,662 chromosomes. There were 300 peripheral blood cell divisions in normal controls, accounting for 13,800 chromosomes. The results showed that the frequencies of kinetochore deletion and kinetochore hysterisis were significantly increased in HEP-2 cells compared with normal human peripheral blood cells (P <0.01), while there was no significant difference in kinetochore-NOR fusion frequency (P> 0.05) The results suggest that kinetochore deletion and kinetochore hysteresis replication may be one of the causes of HEP-2 cell chromosome aneuploidy mutation origin. In addition, we also observed multiple kinetochore phenotypes on some HEP-2 cell chromosomes and suggested that chromosomal multiple kinetochores may be a new pathway for chromosomal structural aberrations in malignant cells.