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目的:以反义寡核苷酸技术研究microRNA-17-5p(miR-17-5p)对人慢性髓系白血病K562细胞增殖的影响及其可能的机制。方法:脂质体法将miR-17-5p反义寡核苷酸(miR-17-5p antisense oligonucleotide,miR-17-5p-ASO)和对照无义寡核苷酸(control nonsense oligonucleotide,Ctrl-NSO)转染入K562细胞,同时设未转染对照组(Ctrl)。MTT法检测K562细胞的增殖,TUNEL法检测K562细胞的凋亡,流式细胞术检测K562细胞周期的改变。结果:MTT检测结果显示,miR-17-5p-ASO组K562细胞增殖活性为Ctrl-NSO组的(61.7±4.7)%,miR-17-5p-ASO转染显著抑制K562细胞的增殖(P<0.05)。TUNEL检测显示,miR-17-5p-ASO转染不影响K562细胞凋亡(P>0.05);miR-17-5p-ASO组K562细胞G2期细胞比例为(10.8±0.8)%,显著低于Ctrl-NSO组和Ctrl组的(34.6±0.4)%和(33.9±1.3)%(P<0.05)。结论:MiR-17-5p反义寡核苷酸可以通过调控细胞周期抑制K562细胞的增殖,有望成为白血病治疗的新手段。
Objective: To study the effect of microRNA-17-5p (miR-17-5p) on proliferation of human chronic myeloid leukemia K562 cells and its possible mechanism by antisense oligonucleotide technique. Methods: The miR-17-5p antisense oligonucleotide (miR-17-5p-ASO) and control nonsense oligonucleotide (Ctrl- NSO) into K562 cells, at the same time set untransfected control group (Ctrl). The proliferation of K562 cells was detected by MTT assay. The apoptosis of K562 cells was detected by TUNEL assay. The cell cycle of K562 cells was detected by flow cytometry. Results: MTT assay showed that the proliferation of K562 cells in miR-17-5p-ASO group was (61.7 ± 4.7)% in Ctrl-NSO group, and miR-17-5p-ASO transfection significantly inhibited the proliferation of K562 cells (P < 0.05). TUNEL assay showed that the miR-17-5p-ASO transfection did not affect the apoptosis of K562 cells (P> 0.05). The proportion of cells in G2 phase in miR-17-5p-ASO group was (10.8 ± 0.8)%, which was significantly lower than (34.6 ± 0.4)% and (33.9 ± 1.3)% (P <0.05) of the Ctrl-NSO and Ctrl groups, respectively. Conclusion: MiR-17-5p antisense oligonucleotide can inhibit the proliferation of K562 cells by regulating the cell cycle and is expected to be a new treatment for leukemia.