【摘 要】
：
目的:在前期体外实验的基础上,进一步检测反义寡核苷酸Glut-1 (Glut-1 AS-ODN)在体内对实体瘤的治疗效果,明确喉癌放射抵抗与Glut-1表达增高有关;并i究LY29400、 wortmannin和apigenin等抑制剂阻滞PI3K/Akt信号通路,降低喉癌细胞中Glut-1表达,明确喉癌细胞中PI3K/Akt信号通路调控Glut-1表达对喉癌放射敏感性的影响及机制.方法:在BAL
【机 构】
：
浙江大学医学院附属第一医院耳鼻咽喉科头颈组 浙江大学医学院附属第一医院耳鼻咽喉科头颈组;山西省人民
【出 处】
：
2014第四届全国耳鼻咽喉科医师大会
论文部分内容阅读
目的:在前期体外实验的基础上,进一步检测反义寡核苷酸Glut-1 (Glut-1 AS-ODN)在体内对实体瘤的治疗效果,明确喉癌放射抵抗与Glut-1表达增高有关;并i究LY29400、 wortmannin和apigenin等抑制剂阻滞PI3K/Akt信号通路,降低喉癌细胞中Glut-1表达,明确喉癌细胞中PI3K/Akt信号通路调控Glut-1表达对喉癌放射敏感性的影响及机制.方法:在BALB/c-nude裸鼠建立了Hep-2喉癌细胞的移植瘤模型,分成对照组,LY294002组,wortmannin组,反义Glut-1组,apigenin组,单纯10Gy照射组,LY294002组+反义Glut-1组,wortmannin组+反义Glut-1组,apigenin组+反义Glut-1组,LY294002组+反义Glut-1组+10Gy,wortrnannin组+反义Glut-1组+10Gy,apigenin组+反义Glut-1组+10Gy,LY294002组+10Gy,wortmannin组+10Gy,检测各组瘤体的变化,并通过反义GLUT-1抑制Glut-1表达、 LY29400、 wortmannin和apigenin等抑制剂阻滞PI3K/Akt信号通路,分别通过实时RT-PCR、 WeStern blotting各组GLUT-1、AKT、 PI3K、 CD133 mRNA以及蛋白的表达情况、TUNEL检测裸鼠瘤体组织的细胞凋亡水平.
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