K562和SiHA细胞株经γ-射线照射后细胞周期阻滞与ATM表达量的关系研究

ATM Expression in K562 and SiHA Cell Lines in Relation to Their Cell Cycle Restardation after γ-irradiation

共济失调毛细血管扩张症(ataxiatelangiectasis,AT)是由ATM(ataxiatelangiectasismutant)基因突变所致,其突出特点是对放射线敏感。为探讨K562和SiHA两种肿瘤细胞株ATM表达量与γ射线照射后细胞周期阻滞即自我保护功能之间的关系,应用半定量RTPCR测量它们的ATMmRNA表达,同时以6、10和15Gy60Coγ射线分别照射细胞,并于照射后6、12、24、48及60小时观察细胞周期阻滞现象和凋亡率的变化。结果显示,K562细胞株ATMRNA相对表达量为0.04,而在SiHA细胞株为0.80,SiHA的ATMRNA表达量约为K562的20倍。结论:照射后K562和SiHA细胞株均表现G/M期阻滞,K562细胞周期阻滞即自我保护机制明显比SiHA差。

Ataxia telangiectasis is caused by the mutation of AT gene （ATM） and it is characterized by hypersensitivity to the radiation. In order to investigate the relationship between ATM mRNA expression of K562 and SiHA two kinds of tumor cell lines and their cell cycle restardation after γ-irradiation, their ATM mRNA expressions were measured by semi-quantitive RT-PCR and the cells were irradiated at the dose of 6, l0 and 15 Gy of ^60Co γ ray and the change of the apoptosis and cell cycle arrest phenomenon were observed at the time of 6, 12, 24, 48 and 60 hours after irradiation. The results showed that the ATM mRNA relative expression level of K562 cell line was 0.04, that of SiHA cell line was 0.80, the ATM transcript levels in SiHA cells were 20 times as much as that in K562. In conclusion, the G2/M phase restardation after irradiation was observed in both cell lines, whereas SiHA exhibited a much stronger cell cycle restardation, a self-protection function, than that of K562.