Acute myeloid leukemia (AML) is a highly heterogeneous disease. Exploring the pathogenesis of AML is still an important topic in the treatment of AML. The expression levels of miR-26b-5p and USP48 were measured by qRT-PCR. The expression levels of related proteins were detected by Western blot. Cell proliferation and apoptosis were detected by CCK-8 and flow cytometry, respectively. Coimmunoprecipitation was used to examine the interaction between USP48 and Wnt5a. Bioinformatics analysis showed that high levels of miR-26b-5p and low levels of USP48 were associated with poor prognosis in AML. miR-26b-5p can negatively regulate the expression of USP48. Downregulation of miR-26b-5p inhibited EMT, cell viability and proliferation of AML cells and accelerated apoptosis. Furthermore, the influence of miR-26b-5p inhibition and USP48 knockdown on AML progression could be reversed by a Wnt/β-catenin signaling pathway inhibitor. This study revealed that miR-26b-5p regulates AML progression, possibly by targeting the USP48-mediated Wnt/β-catenin molecular axis to affect AML cell biological behavior.

中文翻译：

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miR-26b-5p 通过调节 USP48 介导的 Wnt/β-Catenin 通路影响急性髓系白血病的进展

急性髓系白血病（AML）是一种高度异质性的疾病。探索AML的发病机制仍然是AML治疗的重要课题。通过qRT-PCR测量miR-26b-5p和USP48的表达水平。 Western blot检测相关蛋白的表达水平。分别采用CCK-8和流式细胞术检测细胞增殖和凋亡。使用免疫共沉淀来检查 USP48 和 Wnt5a 之间的相互作用。生物信息学分析表明，高水平的 miR-26b-5p 和低水平的 USP48 与 AML 预后不良相关。 miR-26b-5p可以负向调节USP48的表达。 miR-26b-5p 的下调会抑制 AML 细胞的 EMT、细胞活力和增殖，并加速细胞凋亡。此外，Wnt/β-连环蛋白信号通路抑制剂可以逆转 miR-26b-5p 抑制和 USP48 敲低对 AML 进展的影响。这项研究表明，miR-26b-5p 可能通过靶向 USP48 介导的 Wnt/β-catenin 分子轴来影响 AML 细胞生物学行为，从而调节 AML 进展。