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Mechanism of apoptosis of human osteosarcoma M-G63 induced by arsenic trioxide

机译:三氧化二砷诱导人骨肉瘤M-G63凋亡的机制

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Objective To observe the apoptosis of osteosarcoma MG-63 cells induced by As_2O_3 and to explore its possible mechanisms. Methods The flowcytometric analysis and transmission electronmicroscope were performed to investigate the inducing apoptosis and inhibitative of As_2O_3 on osteosarcoma MG-63 cells. In order to study mechanism of apoptosis in MG-63 cells treated with As_2O_3, microarray was performed. The down-regulated gene was confirmed by RT-PCR, Northern-blotting. Results After treated with As_2O_3, hypodiploid peak before G0/G1 phase was observed in MG-63 cells through FCM analysis. Loss of microvilli, condensation and fragmentation of nuclear chromatin, condensation of cytoplasmic organelles, dilatation of the endoplasmic reticulum shrinkage of cells and alterations in cell membranes and apoptosis bodies which were observed in MG-63 cells treated with As_2O_3 by transmission electronmicroscope. The results of microarray show that As_2O_3 induced MG-63 cell apoptosis involves down-regulation of IEX-1 and the down-regulated gene is confirmed by RT-PCR and Northern-blotting. Conclusion The results show that As_2O_3 selectively inhibits growth of the solid tumor MG-63 cells by triggering apoptosis and indicates MG-63 induced by As_2O_3 cell apoptosis may through the IEX-1 pathway.
机译:目的观察As_2O_3诱导的骨肉瘤MG-63细胞凋亡及其可能机制。方法采用流式细胞仪和透射电镜观察As_2O_3对骨肉瘤MG-63细胞的诱导凋亡及抑制作用。为了研究As_2O_3处理的MG-63细胞凋亡的机制,进行了微阵列实验。下调的基因通过RT-PCR,Northern印迹证实。结果经As_2O_3处理后,通过FCM分析,在MG-63细胞中观察到G0 / G1期之前的二倍体峰。通过透射电镜观察到MG_263细胞经As_2O_3处理后,微绒毛丧失,核染色质的凝缩和破碎,细胞质细胞器的凝缩,细胞内质网收缩的扩张以及细胞膜和凋亡小体的改变。芯片结果表明,As_2O_3诱导的MG-63细胞凋亡涉及IEX-1的下调,RT-PCR和Northern印迹法证实了该基因的下调。结论结果表明,As_2O_3通过诱导细胞凋亡来选择性抑制实体瘤MG-63细胞的生长,表明As_2O_3细胞凋亡诱导的MG-63可能通过IEX-1途径。

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