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G2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 the growth of chronic myelocytic leukemia K562 cells by antisense oligonucleocide technique. Methods： miR-17-5p antisense oligonucleotide (miR-17-5p-ASO) and control nonsense oligonucleotide (Ctrl-NSO) were transfected into K562 cells by Lipofectamine assay, and un-transfected K562 cells were used as blank group (Ctrl). The proliferation, apoptosis, and cell cycle changes of K562 cells were examined by MTT, TUNEL, and flow cytometry assays, respectively. Results: MTT results showed that the proliferation of K562 cells in miR-17-5p-ASO group was (61.7±4.7)% of that in Ctrl-NSO group, and miR-17-5p-ASO transfection significantly inhibited the proliferation of K562 cells (P<0.05). TUNEL results showed that miR-17-5p-ASO transfection did not affect apoptosis of K562 cells (P>0.05). The ratio of K562 cells in G2 phase was (10.8±08)％ in miR-17-5p-ASO group, which was significantly lower that those in Ctrl-NSO and Ctrl groups (\[34.6±04\]%, \[33.9±1.3\]%, all P<0.05). Conclusion: MiR-17-5p specific antisense oligonucleotide can suppress K562 cells growth by inhibiting cell cycle, which may provide a new way for treatment of leukemia.

国家自然科学基金资助项目（No. 30873017）