RunX3抑制肿瘤作用的分子机制相关进展  

Mechanism and relative signal pathway of RunX3 in tumor sup- pression

作　　者：郑克鸿[1] 陈飞[1] 黄宗海[1] 

机构地区：[1]南方医科大学珠江医院普外科,广州510280

出　　处：《国际外科学杂志》2013年第1期58-61,共4页International Journal of Surgery

摘　　要：RunX3在肿瘤发病机制中的作用是近年来肿瘤研究的热门领域，在多种类型的肿瘤组织中都发现了RunX3的功能性失活。RunX3能够与TGF-β信号传导通路的下游因子相互协同作用，增强后者抑制细胞生长的能力。RunX3还能与Wnt通路的TCF4-β-catenin复合体相结合，抑制该通路的致癌作用。通过上述两种信号传导通路，RunX3还能参与上皮-间质转化的调控过程，甚至对claudin-1蛋白的表达具有直接调控作用。虽然有研究发现RunX3对一部分肿瘤具有致癌作用，但Runx3这种功能性转变的具体机制仍未明确。现结合近年来国内外的文献，主要针对RunX3在抑制肿瘤作用的相关分子机制研究中的重大发现进行简要综述。The study of RunX3 in tumor pathogenesis is a rapidly expanding area of cancer research. Functional inactivation of RunX3 is frequently observed in tumors of diverse origins. RunX3 can bind directly to the TGF-β signaling effectors for synergistic induction, enhancing the growth inhibitory effect of TGF-β signal pathway. Additionally, RunX3 can also bind to the complex TCF4-β-catenin in Wnt signal pathway for inhibiting its tumorigenicity. Through the two signal pathway mentioned above, RunX3 can regulate the epi- thelial mesenchymal transitions process. Moreover, the transcription of claudin- 1 can be directly regulated by RunX3. RunX3 has also been described to have an oncogenic function in a subset of tumors, but how RunX3 switches from tumor suppression to oncogenic activity is yet unknown. This review focuses on summarizing the important findings about the mechanism and relative signal pathway of RunX3 in tumor suppression from the articles published recently.

关 键 词：RUNX3基因 转化生长因子Β WNT蛋白质类 

分 类 号：R730.2[医药卫生—肿瘤]