摘要
目的研究氯通道阻断剂5-硝基-2-(3-苯丙氨基)苯甲酸[5-nitro-2-(3-phenylpropylamino)benzoicacid,NPPB],对人喉癌细胞系Hep-2细胞裸鼠移植瘤细胞外调节激酶(extracellulat regulated kinase,ERK)ERK1/2和AKT1蛋白磷酸化的影响,探讨阻断氯通道对喉癌移植瘤抑制作用的可能机制。方法以人喉癌Hep-2细胞建立裸鼠皮下移植瘤模型,应用不同浓度的NPPB分组进行治疗实验,研究移植瘤生长变化,Westernblot法检测移植瘤ERK1/2和AKT1蛋白磷酸化水平的变化。结果与对照组比较,各治疗组移植瘤ERK1/2和AKT1总蛋白水平无显著性差异,50、100、150μmol NPPB组ERK1/2和AKT1蛋白磷酸化水平明显降低,差异均有显著性,NPPB浓度依赖性地抑制ERK1/2和AKT1蛋白磷酸化。结论体内阻断氯通道可以抑制人喉癌裸鼠移植瘤的生长,其机制可能与抑制移植瘤细胞ERK1/2和AKT1蛋白磷酸化有关。
OBJECTIVE To study the effect of blocking chloride ion channels on the phosphorylated ERK1/2, AKT1 protein levels of the human laryngeal carcinoma xenograft tumors in nude mice. METHODS Hep-2 cells were seeded subcutaneously into the nude mice to establish human laryngeal carcinoma xenograft models and then treated with PBS and different concentration of NPPB respectively. The changes of the xenograft tumors were studied. Western blot was used to determine the phosphorylated ERK1/2, AKT1 protein levels of the xenograft tumor cells. RESULTS The size and mass of the tumors in the experimental groups （50, 100, 150 μmol NPPB） were significantly decreased （P〈0.05） than that in the control group. The expression of total protein of ERK1/2 and Aktl in the xenograft tumors in the experimental groups （50, 100, 150 μmol NPPB） were not significantly （P〉0.05） changed. Compared with the control group, the phosphorylation levels of ERK1/2 and AKT1 in the experimental groups （50, 100, 150 μmol NPPB/ were significantly （P〈0.05） decreased. CONCLUSION Blocking chloride channels could inhibit the growth of laryngeal carcinoma xenograft tumors in nude mice. The mechanism of the effect might be related to down phosphorylation of ERK1/2 and AKT1 protein.
出处
《中国耳鼻咽喉头颈外科》
CSCD
2013年第1期17-20,共4页
Chinese Archives of Otolaryngology-Head and Neck Surgery
基金
河南省卫生科技创新人才(2010141)
河南省高校青年骨干教师资助计划(2010GGJS-120)联合资助
关键词
喉肿瘤
癌
鳞状细胞
氯化物通道
模型
动物
移植瘤
Laryngeal Neoplasms
CarcinomaSquamous Cell
Chloride Channels
Models, Animalxenograft tumor
