连接蛋白43的磷酸化在恶性肿瘤发生机制中的研究进展  

Research progress on the mechanism of phosphorylation of connexin 43 in pathogenesis of malignant tumor

作　　者：赵希伟 刘倩[1] 滕飞 侯林义[2] 张文凯[2] ZHAO Xiwei;LIU Qian;TENG Fei(Shanxi Medical University,Shanxi,Taiyuan 030001,China)

机构地区：[1]山西医科大学,太原市030001 [2]山西医科大学第二医院重症医学科三病区

出　　处：《河北医药》2021年第24期3812-3816,共5页Hebei Medical Journal

基　　金：山西省太原市科技项目(编号:12016905)。

摘　　要：缝隙连接是由连接蛋白形成的细胞间膜通道,通过允许离子和小分子质量的信号分子的转移促进细胞间通讯。近年来,关于癌症与连接蛋白的关系,形成的共识是连接蛋白表达异常及定位异常,导致缝隙连接细胞间通信(GJIC)的丢失,是肿瘤发生的重要驱动力。连接蛋白43是人体脏器组织中表达比较广泛的连接蛋白。Cx43的磷酸化通过信号通路影响缝隙连接的功能,在缝隙连接通道中起重要作用。Cx43在肺癌、肝细胞癌、胃癌以及乳腺癌等恶性肿瘤的发生机制中表达会出现上调或者下降,引起缝隙连接通道功能出现异常,而Cx43的磷酸化是造成上述异常的重要发生机制。基于Cx43的磷酸化在恶性肿瘤的具体发生机制可以为临床提供更加高效的治疗方案。Gap junctions are intercellular membrane channels formed by connexins that promote intercellular communication by allowing the transfer of ions and small molecular weight signal molecules.In recent years,the consensus about the correlation between cancer and connexin is that the abnormal expression and location of connexin lead to the loss of communication(GJIC)between gap junction cells,which is an important driving force of tumorigenesis.Connexin 43 is a widely expressed connexin in human organs and tissues.The phosphorylation of Cx43 affects the function of gap junctions through various signal pathways and plays an important role in gap junction pathways.The expression levels of Cx43 are up-regulated or down-regulated in the pathogenesis of lung cancer,including hepatocellular carcinoma,gastric cancer and breast cancer,which leads to abnormal function of gap junction channels,and the phosphorylation of Cx43 is an important mechanism of these abnormalities.Therefore,the specific mechanism of Cx43-based phosphorylation in malignant tumors can provide a more efficient treatment in clinical practice.

关 键 词：连接蛋白43 磷酸化 缝隙连接 信号通路 发生机制 恶性肿瘤 

分 类 号：R730.2[医药卫生—肿瘤]