本研究旨在探讨miR-133在急性髓系白血病（AML）多药耐药中的作用及分子机制，为AML患者的治疗和预后提供新的理论依据。我们在细胞水平上进行了实验。采用RT-qPCR和Western blotting检测基因和蛋白表达；使用 CCK-8 测定法测量细胞活力；通过流式细胞术检测细胞凋亡；采用双荧光素酶报告基因检测验证miR-133与CXCL12之间的结合。在这项研究中，我们发现 miR-133 在 HL-60/ADR 多药耐药细胞中表达上调。从功能上讲，抑制 miR-133 可减轻 HL-60/ADR 细胞对柔红霉素 (DNR) 的耐药性。 DNR处理的HL-60/ADR细胞中抑制miR-133后，细胞内耐药相关蛋白MRP562和P-gp的表达受到抑制，细胞增殖减少，细胞凋亡增加。从机制上讲，NF-κB信号通路调节HL-60/ADR细胞中miR-133的表达，miR-133靶向CXCL12增强了HL-60/ADR细胞对DNR的抵抗。综上所述，NF-κB信号通路调节miR-133的表达，抑制miR-133的表达可以靶向CXCL12，增加HL-60/ADR细胞对DNR的敏感性。©作者，独家许可Springer Nature B.V. 2024。Springer Nature 或其许可方（例如协会或其他合作伙伴）根据与作者或其他权利持有人的出版协议拥有本文的专有权；作者对本文已接受的手稿版本的自行存档仅受此类出版协议和适用法律的条款的约束。

This study aimed to explore the role and molecular mechanism of miR-133 in multidrug resistance in acute myeloid leukemia (AML) and provide a new theoretical basis for the treatment and prognosis of AML patients. We performed experiments at the cellular level. RT‒qPCR and Western blotting were used to detect gene and protein expression; cell viability was measured with CCK-8 assays; apoptosis was detected via flow cytometry; and a dual-luciferase reporter gene assay was used to verify the binding between miR-133 and CXCL12. In this study, we found that miR-133 was upregulated in HL-60/ADR multidrug-resistant cells. Functionally, the inhibition of miR-133 alleviated the resistance of HL-60/ADR cells to daunorubicin (DNR). After inhibiting miR-133 in HL-60/ADR cells treated with DNR, the expression of the intracellular drug resistance-related proteins MRP562 and P-gp was inhibited, cell proliferation decreased, and apoptosis increased. Mechanistically, the NF-κB signaling pathway regulates the expression of miR-133 in HL-60/ADR cells, and the targeting of CXCL12 by miR-133 enhances the resistance of HL-60/ADR cells to DNR. In conclusion, the NF-κB signaling pathway regulates the expression of miR-133, and inhibiting miR-133 expression can target CXCL12 to increase the sensitivity of HL-60/ADR cells to DNR.© The Author(s), under exclusive licence to Springer Nature B.V. 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.