激活mGlu5通过MAPK信号通路调节肝癌细胞HepG2生长  

Activating mGlu5 Promotes the Growth of HepG2 Cells Through MAPK Signaling Pathway

作　　者：武永乐[1] 谷利[1] 杨荟敏[1] 刘莉[2] 张红[1,3] 

机构地区：[1]首都医科大学细胞生物学系,北京100069 [2]首都医科大学基础医学院,北京100069 [3]首都医科大学神经生物学系,北京100069

出　　处：《中国生物化学与分子生物学报》2012年第4期332-338,共7页Chinese Journal of Biochemistry and Molecular Biology

基　　金：国家自然科学基金(No.81171886;No.30873087;No.30973406);北京市自然科学基金(No.5102011)资助项目~~

摘　　要：代谢型谷氨酸受体5(mGlu5)与神经元存活及脑肿瘤发生关系密切.近年发现,mGlu5在肝组织中有表达,并且在肝的病理过程中发挥重要的调节作用.而mGlu5是否在肝癌中起作用,目前尚未见报道.本研究选用代谢型谷氨酸受体特异性激动剂二羟基苯甘氨酸(dihydroxyphenylglycine,DHPG)处理肝癌细胞HepG2,从而探讨激活mGlu5对肝癌细胞生长的影响及其机制.结果显示,激活mGlu5能够促进HepG2细胞生长,并激活ERK/JNK通路,抑制p38通路,进而激活转录因子CREB/Elk1和NF-κB.本文揭示了MAPK通路可能参与mGlu5对肝癌细胞生长的调控,为临床提供以mGlu5作为药物靶位点的肝癌治疗新思路.Metabotropic glutamate receptor 5（mGlu5） is known to be important for the development of brain tumors.Recent studies showed that mGlu5 receptor was present in liver tissues with pathologic diagnoses,nonetheless,its connection with hepatocellular carcinoma remained unknown.To study the effect of mGlu5 activation in HepG2 cells,dihydroxyphenylglycine（DHPG） was employed for the treatments.The results showed that the activation of mGlu5 promoted HepG2 cell growth.The stimulated ERK/JNK and inhibited p38 signaling have lead to,the activation of transcription factors,including CREB/Elk1 and NF-κB.This study suggested that MAPK signaling pathway was involved in mGlu5-mediated cell growth of hepatocellular carcinoma cells.

关 键 词：代谢型谷氨酸受体5 丝裂原活化蛋白激酶 肝细胞癌 信号转导 

分 类 号：Q2[生物学—细胞生物学]