突变型p53蛋白稳定表达机制的研究进展  

Research progress in stabilization mechanism of mutant p53 protein expression

作　　者：桂思倩 张继虹[1] 罗瑛[1] 

机构地区：[1]昆明理工大学医学院衰老与肿瘤分子遗传学实验室,云南昆明650500

出　　处：《肿瘤》2014年第7期673-677,共5页Tumor

基　　金：国家自然科学基金云南联合基金资助项目(编号:U1132604);国家自然科学基金资助项目(编号:81260501)

摘　　要：野生型p53(wild-type p53,wtp53)是一种抑癌基因,细胞内其蛋白的稳定性受鼠双微体2(mouse double minute 2,MDM2)蛋白的调节,保持在一个较低的水平;但是p53基因突变后其功能即发生改变,从抑癌基因转变成了对肿瘤发生和发展起促进作用的癌基因,且在肿瘤中高表达。因此,突变型p53(mutant type p53,mtp53)已经成为肿瘤治疗中一个重要的靶点。研究显示,mtp53蛋白的稳定性对其表达并行使功能具有重要作用。因此,了解mtp53蛋白稳定表达的途径,即可为下调mtp53的表达提供一些新的靶点,为肿瘤治疗提供新的途径。本研究旨在对影响mtp53蛋白稳定性的可能途径作一综述。Wild type p53 （wtp53） is a tumor suppressor gene, and the stability of p53 protein expression in cells is regulated by mouse double minute 2 （MDM2） protein and keeps at a low level. However, when the p53 gene is mutant, it can gain the function to promote the generation and progression of tumors and is highly expressed in tumor cells. Therefore, mutant p53 （mtp53） has become an attractive target for cancer therapy. The stability of mutant p53 protein has an important role in its functions. Hence, the understanding of the way of mtp53’s stable expression can provide not only a new target for the degradation of mtp53 protein expression, but also a new strategy for cancer therapy. This review summarizes the research progress in stabilization mechanism of mtp53 protein expression.

关 键 词：肿瘤 基因 p53 HSP90热休克蛋白质类 自噬 组蛋白脱乙酰基酶类 

分 类 号：R730.231[医药卫生—肿瘤]