Objective: To investigate the effect of miR-29b-3p on apoptosis and proliferation of acute myeloid leukemia (AML) cells by targeting signal transducer and activator of transcription 3 (STAT3).
Methods: TargetScan and miRanda online databases were used to predict the binding sites of miR-29b-3p and STAT3 3'UTR. The targeting relationship between them was estimated by Dual-Luciferase reporter assay experiment. After miR-29b-3p over-expression, qPCR and Western blot were used to detect the expression of STAT3 mRNA and proteins, flow cytometry to determine the apoptosis of AML cells, and MTS to detect the changes of cell proliferation in each group.
Results: Dual-Luciferase reporter assay confirmed that STAT3 was the target gene of miR-29b-3p. After miR-29b-3p overexpression, the expression of STAT3 mRNA and protein decreased. Compared with the control groups, the proliferation of AML cells in the overexpression group decreased and the apoptosis increased (P<0.05).
Conclusion: MiR-29b-3p can inhibit the proliferation and induce apoptosis of AML cells by down-regulating STAT3.
题目: miR-29b-3p靶向调控STAT3对AML细胞增殖及凋亡的影响.
目的: 探讨miR-29b-3p通过靶向调控信号转导和转录激活因子3（STAT3）对急性髓系白血病（AML）细胞增殖及凋亡的影响.
方法: TargetScan及miRanda在线数据库预测miR-29b-3p与STAT3 3′UTR区的结合位点，采用双荧光素酶报告基因实验检测二者的靶向关系。qPCR及Western blot检测慢病毒过表达miR-29b-3p后AML细胞miR-29b-3p与STAT3 mRNA及蛋白表达变化，采用MTS检测各组AML细胞增殖变化，流式细胞术检测细胞凋亡情况.
结果: STAT3的3′UTR区存在与miR-29b-3p的结合位点，双荧光素酶报告基因实验证实STAT3是miR-29b-3p的靶基因。慢病毒过表达miR-29b-3p后，STAT3 mRNA及蛋白表达降低，过表达组AML细胞增殖减缓且凋亡增加（P<0.05）.
结论: miR-29b-3p可靶向下调STAT3从而抑制AML细胞增殖，诱导细胞凋亡.