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文章简介快速增殖的白血病前体细胞需消耗大量的葡萄糖,这会导致骨髓中葡萄糖不足。为对抗葡萄糖不足,急性髓系白血病(AML)细胞可上调果糖转运子GLUT5表达而利用果糖。值得注意的是,GLUT5的编码基因SLC2A5高表达、或果糖利用能力增强,均可导致AML患者预后变差。使用小分子药物抑制AML细胞的果糖摄取可明显改善白血病恶性表型,以及增强白血病化疗药物Ara-C的疗效。
INTRODUCTION Rapidly proliferating leukemia precursor cells consume large amounts of glucose, which leads to insufficient glucose in the bone marrow. To combat glucose deficiency, acute myeloid leukemia (AML) cells utilize fructose by up-regulating the expression of GLUT5, a fructose transporter. It is noteworthy that, high GLUT5 gene SLC2A5 expression, or fructose utilization ability, can lead to poor prognosis in patients with AML. Using small molecule drugs to inhibit the fructose uptake of AML cells can significantly improve the malignant phenotype of leukemia and enhance the efficacy of leukemia chemotherapy drug Ara-C.