G蛋白偶联受体37(GPR37)上调促进人胶质瘤U251细胞的增殖  

Up-regulation of GPR37 promotes the proliferation of human glioma U251 cells

作　　者：张亚萍 王礼兴[1] ZHANG Yaping;WANG Lixing(Central Laboratory,Second Affiliated Hospital of Fujian Medical University,Quanzhou 352000,China)

机构地区：[1]福建医科大学附属第二医院中心实验室,福建泉州362000

出　　处：《细胞与分子免疫学杂志》2018年第4期341-345,共5页Chinese Journal of Cellular and Molecular Immunology

基　　金：福建省卫计委青年基金(2015-1-57);福建医科大学附属第二医院苗圃基金(2013MP03)

摘　　要：目的探讨G蛋白偶联受体37(GPR37)表达上调对人胶质瘤U251细胞增殖的影响。方法构建携带GPR37基因的重组质粒,采用脂质体转染法在U251细胞上调表达GPR37,采用实时荧光定量PCR检测GPR37 mRNA水平,Western blot法检测GPR37、磷酸化的蛋白激酶B[p-AKT(Ser473)]蛋白水平,CCK-8法检测U251细胞增殖情况,流式细胞术检测U251细胞的细胞周期。结果与阴性对照组相比,过表达GPR37组细胞的GPR37 mRNA和蛋白水平显著提高。上调细胞的GPR37水平后,明显增加U251细胞的增殖、G1/G0期细胞比例降低,S期和G2期细胞比例升高,并增加p-AKT(Ser473)蛋白水平。结论上调U251细胞的GPR37水平可加速U251细胞周期进程、活化AKT途径并促进细胞增殖。Objective To investigate the impact of up-regulated G protein-coupled receptor 37（ GPR37） on the proliferation of human glioma U251 cells. Methods The recombinant plasmid of GPR37 gene was constructed and transfected into U251 cells by liposome to up-regulate the expression of GPR37. Real-time quantitative PCR was used to detect the mRNA level of GPR37; Western blotting was used to detect the protein levels of GPR37 and phosphorylated AKT[p-AKT（ Ser473） ]; CCK-8 assay was used to detect the proliferation of U251 cells; and flow cytometry was performed to detect the cell cycle of U251 cells. Results Compared with the negative control group,the mRNA and protein levels of GPR37 in GPR37 overexpressing cells significantly increased. After up-regulating GPR37 in U251 cells,we found that the proliferation of U251 cells significantly increased,that the proportion of G1/G0 phase cells decreased,that the proportion of cells in S phase and G2 phase increased,and that the level of p-AKT（ Ser473） was enhanced. Conclusion Up-regulation of GPR37 in U251 cells can accelerate U251 cell cycle progression,activate AKT pathway and promote cell proliferation.

关 键 词：G蛋白偶联受体37(GPR37) 胶质瘤 U251细胞 细胞增殖 细胞周期 

分 类 号：R739.41[医药卫生—肿瘤] Q244[医药卫生—临床医学]