三氧化二砷诱导K562细胞凋亡过程中Par-4及WT1基因表达的变化

Changes of the expression level of Par-4 and WT1 genes during K562 cell apoptosis induced by arsenic trioxide

目的探讨三氧化二砷（As2O3）诱导K562细胞凋亡过程中前列腺凋亡反应因子-4（Par-4）和WT1基因表达的变化。方法用不同浓度As2O3（2～10μmol／L）处理K562细胞24～72h，MTT法测定细胞增生活力，流式细胞术检测细胞凋亡，采用荧光定量RT—PCR检测Par-4和WT1基因mRNA表达变化，Western blotting检测Par-4和WT1蛋白表达的变化。结果不同浓度As2O3作用于K562细胞，随浓度增加能明显抑制细胞的生长，诱导细胞发生凋亡。同时Par-4基因mRNA和蛋白表达逐渐增加；而WT1基因mRNA及蛋白表达逐渐下降。结论As2O3可抑制K562细胞生长，诱导细胞凋亡，Par-4与WT1基因可能参与As2O3诱导K562细胞凋亡的调控。

Objective To explore the changes of Par-4 and WT1 genes expression during human leukemic K562 cells apoptosis induced by arsenic trioxide （As2O3）. Methods After the K562 cells were treated with arsenic trioxide （2-10 μmol/L） for 24-72 hours, cell survival rate was evaluated by MTr assay and apoptosis was analyzed using flow cytometry. The expressions of mRNA and protein for par-4 and WT1 were tested by Real-time quantitative reverse transcriptase polymerase chain reaction （RQ-RT-PCR） method and Western blotting in K562 cells with various concentrations of arsenic trioxide at different time points. Results After the K562 cells were treated with As2O3 of different concentrations, arsenic trioxide could efficiently inhibit the growth of K562 cells and induce apoptosis with the increase of As2O3 concentration. The same time, the mRNA and protein expressions of Par-4 were up-regulated, while the mRNA and protein expression of WT1 were down-regulated. Conclusion Arsenic trioxide could inhibit the growth of K562 cells and induce apoptosis. Par-4 and WT1 genes could participate in the apoptosis of K562 cells induced by arsenic trioxide.