论文部分内容阅读
[目的]研究硒化壳聚糖(Sc)对急性早幼粒细胞白血病(APL)细胞株NB4增殖的影响,探讨这种影响与PML-RARα融合蛋白及其激活的Ras信号途径的关系。[方法]NB4为表达PML-RARα融合蛋白阳性的细胞株,K562为表达PML-RARα融合蛋白阴性的细胞株,应用MTT法检测Sc对两种细胞株增殖的影响,应用流式细胞术和Western blot法检测两种细胞株蛋白含量的变化。[结果]Sc对两种细胞株均可产生剂量和时间依赖性的抑制作用,相比之下,对K562细胞的抑制作用明显较弱(P﹤0.05)。Sc处理后,NB4细胞内PML-RARα融合蛋白和c-Jun信号蛋白含量明显减少,而K562细胞c-Jun信号蛋白含量则轻微减少。[结论]Sc可特异性地减少PML-RARα融合蛋白含量从而下调其激活的Ras信号途径,最终抑制NB4细胞增殖。
[Objective] To investigate the effect of selenium chitosan (Sc) on the proliferation of acute promyelocytic leukemia (APL) cell line NB4 and to explore the relationship between this effect and the PML-RARα fusion protein and its activated Ras signaling pathway. [Method] NB4 was a positive cell line expressing PML-RARα fusion protein and K562 was a negative cell line expressing PML-RARα fusion protein. The effect of Sc on the proliferation of both cell lines was detected by MTT assay. Flow cytometry and Western blot method to detect the changes of protein content in the two cell lines. [Results] Sc both inhibited the proliferation of both cell lines in a dose-and time-dependent manner. In contrast, the inhibitory effect of Sc on K562 cells was significantly weaker (P <0.05). After treatment with Sc, the content of PML-RARα fusion protein and c-Jun signal protein in NB4 cells decreased significantly, while the content of c-Jun signal protein in K562 cells decreased slightly. [Conclusion] Sc can specifically decrease the content of PML-RARα fusion protein and down-regulate the Ras signaling pathway, eventually inhibiting the proliferation of NB4 cells.