急性骨髓性白血病（AML）是一种异质性克隆性疾病，由众多白血病细胞与其微环境中的支持因子之间的复杂相互作用所致。在此背景下，细胞外囊泡（EVs）已被证明在形成肿瘤保护型微环境中扮演了至关重要的角色。本研究考察了AML来源的EVs对骨髓间充质干细胞（BM-MSCs）的细胞和分子特性的影响，特别是与复发和化学耐药相关的基因（IL-6、Gas-6和Galectin-3）表达的改变。MSCs和不同浓度的AML-EVs共培养。我们通过MTT试验、ROS试验、增殖试验和凋亡试验得到了数据。RT-qPCR也用于基因表达分析。我们的结果表明，AML-EVs以浓度依赖的方式影响MSCs的特性。我们发现，在用40 µg/mL的EVs处理后，MSCs的细胞存活率较高，Ki-67和BCL-2增加，ROS水平降低。另一方面，在用60 µg/mL的EVs处理后，MSCs的凋亡率和BAX表达量升高，与对照组相比增加。此外，RT-qPCR结果显示，用40 µg/mL的EVs处理的MSCs中IL-6、Gas-6和Galectin-3的表达显著上调。因为IL-6、Gas-6和Galectin-3的过度表达导致了化疗耐药和复发，我们的研究表明，AML-EVs促使MSCs表达这些基因，从而可能保护白血病细胞免受化疗的伤害，并最终导致复发。版权所有 © 2023。Elsevier Inc.出版。

Acute myeloid leukemia (AML) is a heterogeneous clonal disorder resulting from a complex interplay between leukemic cells and supporting factors from their microenvironment. In this context, extracellular vesicles (EVs) have been shown to play an essential role in forming a tumor-protective microenvironment. In this study, we examined the influence of AML-derived EVs on cellular and molecular characterization of bone marrow mesenchymal stromal cells (BM-MSCs), particularly alteration in the expression of genes (IL-6, Gas-6, and Galectin-3) relating to relapse and chemoresistance.MSCs were co-cultured with different concentrations of AML-EVs. Our data has been achieved by MTT assay, ROS assay, proliferation assay and apoptosis assay. RT-qPCR was also performed for gene expression analysis.Our results demonstrated that AML-EVs impact the MSCs characterization in a concentration-dependent manner. We revealed higher viability, increased Ki-67 and BCL-2, and lower ROS levels in MSCs treated with a 40 µg/mL dose of EVs. On the other hand, the rate of MSCs apoptosis and BAX expression exposed to a 60 µg/mL dose of EVs were increased compared with the control group. In addition, RT-qPCR results showed that the expression of IL-6, Gas-6, and Galectin-3 was significantly up-regulated in treated MSCs with a 40 µg/mL dose of EVs.Because the overexpression of IL-6, Gas-6, and Galectin-3 has contributed to chemoresistance and relapse, our findings suggest that AML-EVs propel MSCs to express these genes, which in turn could guard leukemic cells from chemotherapy-inflicted damages and eventually lead to relapse.Copyright © 2023. Published by Elsevier Inc.