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目的研究S-三苯甲基-L-半胱氨酸(STLC)对慢性粒细胞白血病K562细胞有丝分裂阻滞和凋亡的影响,探讨药物阻滞和凋亡机制及Eg5与bcr/abl信号通路联系。方法将K562细胞分成不加药对照组和不同剂量STLC加药组,药物作用一定时间后,用MTT法检测其对K562细胞的抑制效应,流式细胞术分析细胞周期和亚二倍体峰的变化,Annexin-v/PI双染检测药物处理前后细胞凋亡比率,共聚焦显微镜观察纺锤体与细胞核空间位置关系及凋亡诱导因子(AIF)位移情况,小分子抑制剂阻断结合RT-PCR研究Eg5与bcr/abl信号通路联系。结果STLC可显著抑制K562细胞生长;药物处理早期可阻滞细胞周期进程于G2/M期,且85.5%细胞纺锤体结构呈单星状排列,处理晚期可致细胞凋亡且不依赖于AIF的参与;K562细胞中Eg5表达由bcr/abl酪氨酸激酶所调节。结论STLC诱导K562细胞阻滞在G2/M期并致其凋亡,显示较强的抗有丝分裂和抗肿瘤效果。
Objective To investigate the effects of S-trityl-L-cysteine (STLC) on mitosis arrest and apoptosis in chronic myeloid leukemia K562 cells and explore the mechanisms of drug block and apoptosis and the effects of Eg5 and bcr / abl signaling pathway contact. Methods K562 cells were divided into two groups: drug-free control group and STLC-treated group. After a certain period of treatment, the inhibitory effect of K562 cells on K562 cells was detected by MTT assay. The cell cycle and subdiploid peak were analyzed by flow cytometry The apoptotic rate of AIF was detected by confocal microscopy. The relationship between spindle and nucleus spatial location and the expression of AIF was observed by Annexin-v / PI double staining. The binding of small molecule inhibitors to RT-PCR Study Eg5 and bcr / abl signaling pathway. Results STLC could significantly inhibit the growth of K562 cells. At the early stage of drug treatment, cell cycle progression was blocked at G2 / M phase. The structure of 85.5% spindle cells was arranged in a single star shape. The cells treated with STLC could induce apoptosis and did not depend on AIF Participation; Eg5 expression in K562 cells is regulated by bcr / abl tyrosine kinase. Conclusion STLC can induce the apoptosis of K562 cells in G2 / M phase, which shows strong anti-mitotic and anti-tumor effect.