婴儿血管瘤发病率高，病程长，严重影响儿童生理和心理健康。治疗婴儿血管瘤的关键在于发病增生期控制瘤体生长速度，在消退期加速其凋亡及细胞分化。课题组前期研究发现，GLUT1在血管瘤中表达量从增生期到消退期逐渐下调，IGFⅡ/IGF2R及AKT/PI3K通路在增生期血管瘤中异常活化，且IGFⅡ/IGF2R和 AKT/PI3K通路均参与血管瘤的增殖、凋亡的调控。同时，我们通过GFP标记GLUT1阳性的血管瘤干细胞，发现其是消退期脂肪细胞的主要来源。GLUT1在多种癌症中参与调控增殖、凋亡，而其在血管瘤中的作用机制尚未报道。因此，我们推断GLUT1参与调控婴儿血管瘤增殖、凋亡及分化。本研究拟从临床标本、细胞、分子以及动物实验水平来验证，GLUT1通过HIF-1α/P53、IGF2/AKT/PI3K及HIF-1α/AKT通路调控婴儿血管瘤增殖凋亡及分化，以期为婴儿血管瘤临床治疗找到新的突破口。

Infantile hemangioma is a blood vessel proliferative disease with high incidence, long duration. It has serious influence on children's physical and mental health. The key for the treatment of infantile hemangioma is to limit tumor growth in the proliferating period, and enhance apoptosis and cell differentiation in the involuting period. Our previous study found that the expression of GLUT1 in hemangioma decreased during the transition from proliferating to involuting, in which IGFⅡ/IGF2R and AKT/PI3K pathway were both activated in the proliferating period of hemangioma, and they were involved in proliferation and apoptosis of hemangioma. In addition, our study using GFP labled GLUT1 positive hemangioma stem cells demonstrated that it was the main source of adipocyte in the involuting period of hemangioma. GLUT1 is involved in the regulation of proliferation and apoptosis in various types of tumors. however, its role in the regulatory pathway of hemangioma has not been reported. Based on our findings, we hypothesized that GLUT1 could regulate the proliferation, apoptosis and differentiation in infantile hemangioma. Our research project aims to verify the regulatory mechanism of GLUT1 through HIF-1α/P53,IGF2/AKT/PI3K and HIF-1α/AKT pathway in proliferation, apoptosis and differentiation of infantile hemangioma using cellular, animal model and clinical samples which will facilitate to address the regulatory mechanism involved in the formation of infantile hemangioma and novel therapeutic measures.