急性髓细胞白血病（AML）是一类因基因异常导致的血液系统恶性疾病。近年来的研究表明，紊乱的代谢在AML的发生发展中也起着重要的作用。我们之前发现，AML细胞的糖代谢活跃，消耗葡萄糖的速率快，因此可导致骨髓微环境中葡萄糖不足。此时，AML细胞可上调果糖转运子蛋白GLUT5表达、转向利用血液系统中的第二大血糖--果糖。由GLUT5介导的、增强的果糖利用，可强烈激活AML细胞的糖酵解代谢、导致糖代谢发生重编程，进而促进细胞增殖、增强细胞的集落形成/移动/浸润能力。对于果糖驱动的糖代谢重编程如何导致AML细胞增殖和存活，相关分子机制尚未明确。基于前期实验，我们提出这样的科学假说：果糖驱动的糖代谢重编程，可促进AML细胞中ROS的生成，ROS作为信号分子激活PI3K/AKT信号通路，促进AML细胞增殖和存活。本研究将为我们通过干预果糖代谢治疗AML提供坚实的科学依据。

Acute myeloid leukemia (AML) is a group of hematological neoplasms caused by genetic aberrations. Recent studies show that altered metabolism also plays an essential role in the initiation and development of AML. We demonstrated previously that AML cells with a metabolic feature of highly active glucose metabolism consumed substantial glucose, thus resulting in glucose insufficiency in the bone marrow. Under this condition, AML cells switched to utilize fructose via upregulating the fructose transporter GLUT5. It is known that fructose is the second most abundant blood sugar in humans. We showed that enhanced fructose utilization mediated by GLUT5 was able to strongly activate glycolytic flux in AML cells, thus promoting cell proliferation, elevating colony growth, and increasing migratory and invasive tendency. However, it is still unclear what is the molecular mechanism used by fructose-driven glucose metabolism reprogramming to promote AML cell proliferation and survival. Based on preliminary results, we hypothesize that fructose-driven glucose metabolism reprogramming is able to promote ROS production. Furthermore, we suppose that ROS can activate PI3K/AKT signaling, thus promoting AML cell proliferation and survival. This study will uncover the potential mechanism used by fructose-driven glucose metabolism reprogramming to promote AML cell neoplastic growth, and provide us with new evidence for fructose metabolism pathway as a potential therapeutic target for AML.