Acute myeloid leukemia (AML) is a prevalent class of blood disease with a high occurrence rate and relapse rate. The role of dysregulated microRNAs (miRNAs) in AML is emerging. MiR-4260 was identified to be a carcinogenic miRNA in colorectal cancer, but never has it been reported in AML. We aimed to study the function and mechanism of miR-4260 in AML. The miR-4260 level was higher in AML cell lines than the normal cell lines. Inhibition of miR-4260 hindered proliferation and increased apoptosis of AML cells. Mechanistically, long intergenic non-protein coding RNA 1128 (LINC01128) competed with nuclear receptor subfamily 3 group C member 2 (NR3C2) for miR-4260 so as to upregulate NR3C2. We identified the reduced levels of LINC01128 and NR3C2 in AML and it was suggested through rescue assays that LINC01128 repressed AML progression through regulating miR-4260/NR3C2 axis. In conclusion, we firstly uncovered that LINC01128 resisted acute myeloid leukemia through regulating miR-4260/NR3C2, providing novel clues for the treatment improvement of AML.

急性髓系白血病（AML）是一类发病率高、复发率高的血液病。异常调节的微小 RNA (miRNA) 在 AML 中的作用正在显现。MiR-4260 被鉴定为结直肠癌中的致癌 miRNA，但从未在 AML 中报道过。我们旨在研究 miR-4260 在 AML 中的功能和机制。AML 细胞系中的 miR-4260 水平高于正常细胞系。抑制 miR-4260 会阻碍 AML 细胞的增殖并增加其凋亡。从机制上讲，长基因间非蛋白质编码 RNA 1128 (LINC01128) 与核受体亚家族 3 C 组成员 2 (NR3C2) 竞争 miR-4260，从而上调 NR3C2。我们确定了 AML 中 LINC01128 和 NR3C2 水平的降低，并且通过救援试验表明，LINC01128 通过调节 miR-4260/NR3C2 轴来抑制 AML 进展。总之，我们首次发现LINC01128通过调节miR-4260/NR3C2来抵抗急性髓系白血病，为改善AML的治疗提供了新的线索。