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在抗VEGF耐火性瘤中,依赖于糖化酶的莱克受体相互作用可保持血管生成

Diego O Croci¹, Juan P Cerliani¹, Tomas Dalotto-Moreno¹

¹Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), 1428 Buenos Aires, Argentina.

|February 18, 2014

概括

瘤对抗血管内皮生长因子 (VEGF) 疗法产生耐药性,通过改变细胞表面的糖来结合加勒-1 (Gal1),这推动了血管生长. 针对这种糖化化途径可以恢复对抗VEGF治疗的敏感性.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

血管内皮生长因子 (VEGF) 向治疗的临床益处通常受瘤耐药性限制.
抗VEGF治疗后瘤再生表明血管生成的补偿机制.

研究的目的:

为了确定促进血管生成和瘤抵抗VEGF阻塞的依赖于糖化酶的途径.
探索向莱克受体相互作用,以提高抗VEGF治疗的疗效.

主要方法:

在对VEGF阻塞的反应中分析了内皮细胞 (EC) 表面糖体重塑.
研究了加勒-1 (Gal1) 通过N-glycans与VEGFR2结合的作用.
评估了改变糖化模式 (例如,酸,β1-6GlcNAc分支) 和Gal1水平对瘤对抗VEGF治疗的反应的影响.

主要成果:

瘤对抗VEGF治疗的耐药性是由一个涉及EC表面糖体重塑和与VEGFR2结合的加勒-1 (Gal1) 结合的途径中介的.
抗VEGF敏感的瘤具有高α2-6结合的酸,防止Gal1结合,而耐火瘤显示Gal1增加和允许的糖化.
干扰Gal1-N-甘氨酸相互作用或降低Gal1水平将耐火性瘤转化为抗VEGF敏感状态.
破坏Gal1-N-甘氨酸轴促进了血管重塑,免疫细胞透,并抑制了瘤生长.

结论:

与VEGFR2的糖化依赖的加勒-1 (Gal1) 相互作用代表了瘤对抗VEGF治疗耐药性的关键机制.
针对Gal1-N-glycan轴提供了一个有希望的策略,以克服耐药性并提高抗VEGF治疗的疗效.

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