目的 探讨微小RNA（miRNA, miR）-100-5p靶向Tribbles同源蛋白1（Tribbles pseudokinase 1, TRIB1）对急性髓系白血病细胞增殖及凋亡活性的影响。 方法 收集16例健康体检儿童（对照组）和16例AML患儿（AML组）外周血。将HL-60细胞分为空白组、mimic NC组、miR-100-5p mimic组、si-NC组、si-TRIB1组、miR-100-5p mimic+TRIB1过表达质粒阴性对照（OE-NC）组、miR-100-5p mimic+TRIB1过表达质粒（OE-TRIB1）组。采用实时荧光定量PCR检测外周血和HL-60细胞中miR-100-5p、TRIB1 mRNA表达；5-乙炔基-2'脱氧尿嘧啶核苷（5-ethynyl-2'-deoxyuridine, EdU）染色、CCK-8法检测HL-60细胞增殖；流式细胞术检测HL-60细胞凋亡；Western blot法检测HL-60细胞中TRIB1、增殖细胞核抗原（proliferating cell nuclear antigen, PCNA）、p53、程序性死亡受体-1（programmed cell death protein 1, PD-1）、程序性死亡受体-配体1（programmed death-ligand 1, PD-L1）蛋白表达；双萤光素酶报告基因实验验证miR-100-5p与TRIB1靶向关系。 结果 与对照组比较，AML组外周血中miR-100-5p表达降低，TRIB1 mRNA表达升高（P<0.05）。与空白组、mimic NC组比较，miR-100-5p mimic组miR-100-5p表达、细胞凋亡率、p53蛋白表达升高，TRIB1 mRNA表达、EdU阳性率、光密度（optical density, OD）₄₅₀值及TRIB1、PCNA、PD-1、PD-L1蛋白表达降低（P<0.05）；与空白组、si-NC组比较，si-TRIB1组TRIB1 mRNA表达、EdU阳性率、OD₄₅₀值及TRIB1、PCNA、PD-1、PD-L1蛋白表达降低，细胞凋亡率、p53蛋白表达升高（P<0.05）；与miR-100-5p mimic组、miR-100-5p mimic+OE-NC组比较，miR-100-5p mimic+OE-TRIB1组TRIB1 mRNA表达、EdU阳性率、OD₄₅₀值及TRIB1、PCNA、PD-1、PD-L1蛋白表达升高，细胞凋亡率、p53蛋白表达降低（P<0.05）；TRIB1-WT + miR-100-5p mimic组萤光素酶活性低于TRIB1-WT + mimic NC组（P<0.05）。 结论 过表达miR-100-5p可通过下调TRIB1抑制HL-60细胞增殖，诱导细胞凋亡。

Objective To investigate whether miR-100-5p regulates the proliferation and apoptosis of acute myeloid leukemia (AML) cells by targeting Tribbles pseudokinase 1 (TRIB1). Methods Peripheral blood was collected from 16 healthy children (control group) and 16 children with AML (AML group). HL-60 cells were divided into seven groups: blank, mimic negative control (mimic NC), miR-100-5p mimic, small interfering RNA negative control (si-NC), si-TRIB1, miR-100-5p mimic + TRIB1 overexpression plasmid negative control (OE-NC), and miR-100-5p mimic + TRIB1 overexpression plasmid (OE-TRIB1). The expression of miR-100-5p and TRIB1 mRNA in peripheral blood and HL-60 cells was detected by quantitative real-time PCR. Cell proliferation was assessed by 5-ethynyl-2'-deoxyuridine (EdU) staining and the cell counting kit-8 (CCK-8) assay (OD₄₅₀). Apoptosis was analyzed by flow cytometry. Protein levels of TRIB1, proliferating cell nuclear antigen (PCNA), p53, programmed cell death protein 1 (PD-1), and programmed death-ligand 1 (PD-L1) were determined by Western blot. The targeting relationship between miR-100-5p and TRIB1 was validated by a dual-luciferase reporter assay. Results Compared with the control group, miR-100-5p expression was decreased and TRIB1 mRNA expression was increased in the peripheral blood of the AML group (P<0.05). Compared with the blank and mimic NC groups, the miR-100-5p mimic group showed higher miR-100-5p expression, apoptosis rate, and p53 protein, and lower TRIB1 mRNA expression, EdU-positive rate, OD₄₅₀ value, and TRIB1, PCNA, PD-1, and PD-L1 proteins (P<0.05). Compared with the blank and si-NC groups, the si-TRIB1 group exhibited reduced TRIB1 mRNA expression, EdU-positive rate, OD₄₅₀ value, and TRIB1, PCNA, PD-1, and PD-L1 proteins, together with increased apoptosis rate and p53 protein (P<0.05). Compared with the miR-100-5p mimic and miR-100-5p mimic + OE-NC groups, the miR-100-5p mimic + OE-TRIB1 group had elevated TRIB1 mRNA expression, EdU-positive rate, OD₄₅₀ value, and TRIB1, PCNA, PD-1, and PD-L1 proteins, and reduced apoptosis rate and p53 protein (P<0.05). Compared with the TRIB1-WT + mimic NC group, luciferase activity was decreased in the TRIB1-WT + miR-100-5p mimic group (P<0.05). Conclusions Overexpression of miR-100-5p inhibits proliferation and induces apoptosis of HL-60 cells by downregulating TRIB1.