P53突变与乳腺癌转移的关系  

Relationship between p53 Mutation and Breast Cancer Metastasis

作　　者：金羽茜 黄文卉[1] 罗瑛[1] 杨昆宪[2] 

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,昆明市650500 [2]云南省第一人民医院乳腺甲状腺肿瘤科,昆明市650500

出　　处：《医学分子生物学杂志》2015年第6期355-360,共6页Journal of Medical Molecular Biology

摘　　要：乳腺癌是女性最常见的癌症之一，其预后与淋巴结转移密切相关。临床上的一些分子标志物可以用来预测淋巴结转移，如：雌激素受体（estrogenreceptor，ER）阴性以及p53突变，人表皮生长因子受体2（humanepidermalgrowthfactorreceptor2，HER-2），Ki-67和血管内皮生长因子（vascular endothelial growthfactor，VEGF）高表达的患者更容易发生淋巴结转移。其中p53作为一个关键的抑癌基因可能与这些生物标志物存在重要的协同或调节作用。当p53发生突变时，失去了对这些生物标志物的正常调控，突变p53蛋白获得的新功能反而促进了淋巴结的转移。在肿瘤浸润、转移的过程中必然会有上皮-间质转化（epithelial-mesenchymalt ransition，EMT）的发生，突变p53也促进了EMT的进程。作者就突变型p53与EMT、ER、HER-2、Ki-67、VEGF的相互作用促进乳腺癌淋巴结转移作一阐述。Breast cancer （BC） is by far one of the most common cancers in women, and its prognosis is closely associated with lymph node metastasis. Some clinical molecular markers can be used to predict lymph node metastasis, such as estrogen receptor （ER） and p53. Patients with high expression of human epidermal growth factor receptor 2 （ HER- 2） , Ki-67 and vascular endothelial growth factor （VEGF） are more likely to develop the lymph node metastasis, p53, a key tumor-sup- pressor gene, may have important synergic or regulative associations with these biomarkers. The p53 mutation may result in the loss of the normal regulation of these biomarkers, leading to the lymph node metastasis. Epithelial-mesenchymal transition （EMT） inevitably occurs in the process of tumor invasion and metastasis, and mutant p53 also promotes the process of EMT. Here, we discuss the interaction of mutant p53 with EMT, ER, HER-2, Ki-67 and VEGF in lymph node metastasis of breast cancers.

关 键 词：乳腺癌 突变P53 淋巴结转移 EMT 生物标志 

分 类 号：R34[医药卫生—基础医学]