[Effect of miR-22 Targeting FMNL2 on Cell Migration and Apoptosis in Childhood Acute Myeloid Leukemia].

To investigate the effect of miR-22 targeting formin-like protein 2 (FMNL2) on the migration and apoptosis of childhood acute myeloid leukemia (AML) cells.Peripheral blood samples from 11 children with AML, 10 children with immune thrombocytopenia, human AML cell lines TF-1a, HL-60, THP-1 and human bone marrow stromal cells HS-5 were used as the research objects. UniCel DxH 800 automatic hematology analyzer detected platelet count, hemoglobin, and white blood cell count in peripheral blood samples, and RT-qPCR detected miR-22 expression in peripheral blood samples and AML cells. HL-60 cells were transfected with LipofectamineTM 2000 kit, the experiments were divided into seven groups: blank (no cells transfected), miR-NC, miR-22 mimics, si-NC, si-FMNL2 , miR-22 mimics+OE-NC and miR-22 mimics+OE-FMNL2 . RT-qPCR was used to detect the expression of miR-22 in each group. Transwell was used to detect cell migration. Flow cytometry was used to detect cell apoptosis. Dual-luciferase reporter gene detection experiments verified the targeting relationship between miR-22 and FMNL2 . Western blot was used to detect the expression of FMNL2 protein.Compared with the control group, the number of leukocytes in the peripheral blood of children with AML was significantly increased (P <0.001), while the concentration of hemoglobin and the number of platelets were significantly decreased P <0.001). The expression level of miR-22 in peripheral blood of children with AML was significantly lower than that in control group (P <0.001). Compared with HS-5 cells, the expression levels of miR-22 in TF-1a, HL-60, and THP-1 cells were significantly decreased (P <0.05), and in HL-60 cells was the lowest. Therefore, HL-60 cells were selected for subsequent experiments. Up-regulation of miR-22 or silencing of FMNL2 could reduce the number of migrating cells and increase apoptosis rate (P <0.05). MiR-22 targeted and negatively regulated the expression of FMNL2 . FMNL2 overexpression reversed the effects of up-regulated miR-22 on migration and apoptosis of HL-60 cells.MiR-22 can inhibit the migration and promote apoptosis of HL-60 cells by down regulating the expression of FMNL2 .miR-22靶向FMNL2 对儿童急性髓系白血病细胞迁移和凋亡的影响.探讨miR-22靶向同源形成素样蛋白2（FMNL2）对儿童急性髓系白血病（AML）细胞迁移和凋亡的 影响。.以11例AML患儿、10例免疫性血小板减少患儿的外周血标本以及人AML细胞系TF-1a、HL-60、THP-1和人骨髓基质细胞HS-5为研究对象，UniCel DxH 800型全自动血液分析仪检测外周血标本的血小板数、血红蛋白、白细胞数，RT-qPCR检测外周血标本和AML细胞中miR-22表达；利用LipofectamineTM 2000试剂盒对HL-60细胞进行转染，实验分为空白（细胞未转染）、miR-NC、miR-22 mimics、si-NC、si-FMNL2 、miR-22 mimics+OE-NC 和miR-22 mimics+OE-FMNL2 共7组，RT-qPCR检测各组细胞miR-22表达；Transwell检测细胞迁移；流式细胞术检测细胞凋亡；双荧光素酶报告基因检测实验验证miR-22与FMNL2 靶向关系；Western blot检测FMNL2蛋白表达 情况。.与对照组比较，AML患儿外周血中白细胞数显著升高（P <0.001），血红蛋白浓度及血小板数显著降低（P <0.001）；AML患儿外周血中miR-22的表达水平显著低于对照组（P <0.001）；与HS-5细胞比较，TF-1a、HL-60、THP-1细胞中miR-22的表达水平均显著降低（P <0.05），且HL-60细胞中的miR-22的表达水平最低，因此，选择HL-60细胞进行后续实验；上调miR-22或沉默FMNL2 均可降低迁移细胞数目，提高细胞凋亡率（P <0.05）；miR-22靶向负调控FMNL2 的表达；FMNL2 过表达逆转了上调miR-22对HL-60细胞迁移和凋亡的影响。.miR-22通过靶向下调FMNL2 表达，抑制HL-60细胞迁移、促进细胞凋亡。.