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了解Wilms肿瘤基因 (WT1)反义寡核苷酸 (ASO)对白血病细胞凋亡的作用。方法 :应用WT1ASO以及足叶乙甙 (VP 16 )作用K5 6 2、HL 6 0细胞系 ,然后应用流式细胞仪测定DNA含量以确定白血病细胞的凋亡数。结果 :K5 6 2细胞系经WT1ASO作用 2 4h和 6 0h后细胞凋亡数分别为 14.6 %和 2 6 .8% ;而WT1有义寡核苷酸 (SO)组分别为 3.1% (2 4h)和 3 9% (6 0h) ;加入少量VP 16后凋亡数达到 37 2 % (2 4h)和 6 6 .6 % (6 0h)。HL 6 0细胞经WT1ASO作用 2 4h及 6 0h后细胞凋亡数无明显增高 ,但作用 6 0h后与VP 16联合作用 ,细胞凋亡可达 34.7% ,大于单用VP 16 (13 .7% )及VP 16 +SO (15 .4% )诱导的细胞凋亡数。结论 :WT1ASO可以导致K5 6 2细胞凋亡并可提高白血病细胞对VP 16的敏感性。WT1基因与白血病细胞的凋亡有关 ,其在不同细胞中所发挥的作用不同。
To investigate the effect of Wilms tumor gene (WT1) antisense oligonucleotide (ASO) on leukemic cell apoptosis. Methods: K562 and HL-60 cell lines were treated with WT1ASO and etoposide (VP 16). The DNA content was determined by flow cytometry to determine the number of apoptotic leukemia cells. Results: The number of apoptotic cells in K562 cells treated with WT1ASO for 24 h and 60 h were 14.6% and 26.8%, respectively, while WT1 sense oligonucleotide (SO) was 3.1% (24 h ) And 39% (60 h) respectively. Apoptosis was 37 2% (24 h) and 66.6% (60 h) after adding a small amount of VP 16. The number of apoptotic cells in HL-60 cells treated with WT1ASO for 24 h and 60 h did not increase significantly, but the combined effect of VP6 and HL-60 cells after 60 h treatment was 34.7%, higher than that of VP 16 (13.7% ) And VP 16 + SO (15.4%) induced apoptosis. Conclusion: WT1ASO can induce apoptosis of K562 cells and increase the sensitivity of leukemic cells to VP16. The WT1 gene is involved in the apoptosis of leukemic cells and plays a different role in different cells.