TMEM16A在肿瘤中高表达的机制  

Mechanism of the overexpression of TMEM16A Ca^(2+)-activated chloride channel in cancer

作　　者：勾睿 王慧[1] 肖庆桓 

机构地区：[1]中国医科大学药学院离子通道药理研究室,沈阳110122

出　　处：《解剖科学进展》2017年第4期436-438,442,共4页Progress of Anatomical Sciences

基　　金：国家自然科学基金(81572613)

摘　　要：TMEM16A在多种肿瘤中高表达,是治疗肿瘤的潜在靶点和生物标记物,但TMEM16A在肿瘤发生发展过程中的作用机制尚未阐明。染色体11q13区扩增、转录调控、表观遗传调控和下调microRNA等因素导致TMEM16A高表达。TMEM16A高表达激活MAPK、EGFR、CaMKII和NFB等信号通路参与肿瘤细胞增殖,凋亡,迁移和侵袭。TMEM16A was found to be overexpressed in many tumors, and a potential target and biomarker for tumor treatment. However, its mechanism in the process of tumor occurrence and progression has not yet been clarified. Chromosome 11q13 region amplification, transcriptional regulation, epigenetic regulation, down-regulation of microRNAs and other factors lead to the overexpression of TMEM16A. TMEM16A overexpression involves in tmnor cell proliferation, apoptosis, migration and invasion by activating MAPK, EGFR, CaMKII, NFB and other signaling pathway. In this review, we summarize recent findings about the mechanisms of TMEM16A overexpression and the signaling pathways activated by TMEM16A in cancer.

关 键 词：肿瘤发生发展 microRNA 表观遗传调控 肿瘤细胞增殖 CAMKII 生物标记物 高表达激活 转录调控 

分 类 号：R730.2[医药卫生—肿瘤]