CD44v6通过Akt信号通路调节胶质瘤细胞生长  

CD44v6 regulates the growth of glioma cells through the Akt signaling pathway

作　　者：胡军[1] 程妮 钟占强[3] 冯华 周建军[3] Hu Jun;Cheng Ni;Zhong Zhanqiang;Feng Hua;Zhou Jianjun(Department of Neurology,Shaanxi People＇s Hospital,Shaanxi Xi＇an 710068,China;Internal Medicine,the Fifth Hospital of Xi＇an,Shaanxi Xi＇an 710082,China;Department of Pain,The 323 Hospital of PLA,Shaanxi Xi＇an 710054,China;Department of Neurosurgery,Southwest Hospital,Army Medical University,Chongqing 400038,China.)

机构地区：[1]陕西省人民医院神经内科,陕西西安710068 [2]西安市第五医院内一科,陕西西安710082 [3]解放军第三二三医院疼痛科,陕西西安710054 [4]陆军军医大学西南医院神经外科,重庆400038

出　　处：《现代肿瘤医学》2018年第19期3021-3025,共5页Journal of Modern Oncology

基　　金：陕西省科学技术研究自然基金(编号:2013JM4006);兰州军区医药卫生科研计划项目(编号:CLZ13JB18);第三二三医院2012年度培育课题(编号:2012323A01)

摘　　要：目的:探讨CD44v6对胶质瘤细胞生长的影响及其相关机制。方法:细胞免疫荧光染色观察A172细胞中CD44v6表达情况及其表达部位。实时荧光定量PCR和Western blot检测A172细胞中CD44v6以及siRNA下调CD44v6表达的情况,MTT检测CD44v6对细胞活力的影响,AnnexinⅤ-FITC/PI染色检测CD44v6对细胞凋亡的影响,Western blot检测细胞中p-Akt水平。结果:A172细胞表达CD44v6,表达部位在细胞膜。siRNA下调CD44v6表达后,细胞生长显著减缓,细胞凋亡增加。CD44v6配体-骨桥蛋白促进A172细胞Akt的磷酸化,下调CD44v6表达后,骨桥蛋白的这种效应被显著抑制。进一步,骨桥蛋白促进A172细胞生长,下调CD44v6表达后,骨桥蛋白促进A172细胞生长的效应消失。结论:CD44v6增加A172细胞活力,抵抗细胞凋亡,其促进细胞内Akt的磷酸化是其中的一个机制。Objective：To investigate the effect of CD44v6 on the growth of glioma cells and its mechanism. Methods：Cell inmmnofluorescence staining was used to detect the expression of CD44v6 and its expression site in A172 cells. Real-time fluorescence quantitative PCR and Western blot were used to detect the expression of CD44v6 in normal and siRNA-treated A172 cells. MTT was used to detect the effects of CD44v6 on A172 cell growth. Annexin V - FITC/PI staining was used to detect the effect of CD44v6 on cell apoptosis. Western blot was used to detect the expression level of p-Akt in A172 cells. Results ： CD44v6 was expressed in cell membrane of A172 cells. There were significantly decreases in the cell growth and apoptosis increases compared in the normal group when CD44v6 was down - regulated by siRNA. Akt phosphorylation was induced by CD44v6 ligand osteopontin,while the above effect of osteopontin was significantly inhibited through down - regulating the expression of CIM4v6 protein by CD44v6 siRNA in A172 cells. Furthermore,osteopontin promoted the growth of A172 cells,while the above effect of osteopontin was also significantly inhibited through down - regulating the expression of CD44v6 protein by CD44v6 siRNA. Conclusion ：CIN4~6 increased the cell viability and resisted apoptosis by promoting the phosphorylation of Akt in A172 cells.

关 键 词：胶质瘤 CD44V6 AKT 

分 类 号：R730.264[医药卫生—肿瘤]