白血病干细胞的生物学特性使其具有自我更新和保持相对静息状态的能力，并且对化疗药物不敏感，是白血病治疗后复发及预后不良的根源。我们的前期研究发现，白血病细胞中Rac1的高度活化有利于白血病细胞干性的维持。作为特异性激活Rac1/Cdc42的鸟苷酸交换因子，ARHGEF6参与调节多种肿瘤的生物学行为。本项目拟以ARHGEF6在白血病细胞中的表达水平与急性髓系白血病患者预后的关系作为研究的切入点，以急性髓系白血病细胞系和患者来源的骨髓细胞以及小鼠白血病模型为研究对象，通过调节白血病细胞中ARHGEF6的表达，确定ARHGEF6是否能够影响白血病细胞的自我更新、静息状态、耐药性等干性相关的生物学功能以及白血病小鼠的生存期，并进一步阐明其发挥作用的分子机制，为AML的发病机制提供理论基础，为白血病的靶向治疗提供新的策略。

The biological characteristics of leukemia stem cells (LSCs) endow LSC the ability of self-renewal capacity, quiescence and chemotherapy insensitivity which is the main reason for recurrence after treatment and poor prognosis of leukemia.In our previous study, we found that activation of Rac1 GTPase plays an important role in stemness maintenance of leukemia cells.As guanine-nucleotide exchange factor to activate Rac1 GTPase and Cdc42, ARHGEF6 can regulate biological behaviours in many cancers. This project will take the relationship between the expression level of ARHGEF6 in leukemia cells and the prognosis of patients with acute myeloid leukemia as the starting point, and take the acute myeloid leukemia cell lines, bone marrow cells from patients and mouse leukemia model as the research object. By regulating the expression of ARHGEF6 in leukemia cells, we can determine whether ARHGEF6 can affect the self-renewal capacity, quiescence, drug resistance of leukemia cells and the survival time of leukemia mice are also discussed. The molecular mechanism of their action is further elucidated to provide a new target for the clinical treatment of leukemia.