LMO2调控E-cadherin启动子的活性对前列腺癌恶化转移的影响  

Regulation of E-cadherin promoter activity by LMO2 impact on the progression and metastasis of prostate cancer

作　　者：彭茜[1] 叶正[1] 高杨[1] 

机构地区：[1]南开大学医学院,天津300071

出　　处：《中国应用生理学杂志》2013年第5期385-389,共5页Chinese Journal of Applied Physiology

基　　金：国家自然科学基金资助项目(81101567);天津市应用基础及前沿技术研究计划(11JCYBJC 12400)

摘　　要：目的:研究原癌基因LMO2异常表达对前列腺癌恶化转移的影响及其可能机制。方法:采用分子克隆技术构建了一系列不同长度和点突变的E-cadherin基因启动子区序列至pGL-3 basic荧光素酶表达载体,然后将这些重组质粒与LMO2表达质粒共转染Lncap细胞并在24 h后检测其荧光素酶活性。结果:过表达LMO2可以显著的抑制E-cadherin启动子荧光素酶报告基因的活性,使荧光素酶活性下降50%左右。通过截短和点突变研究发现其作用机制主要通过结合在启动子区-204/-198处的E-box位点发挥作用。结论:原癌基因LMO2可通过对Ecadherin发挥转录抑制作用来影响前列腺癌的恶化与转移。Objective： To study the abnormal expression of the proto-oncogene LMO2 affect the progression and metastasis mechanism of prostate cancer. Methods： A series of reporter gene expression vectors carrying different lengths and point mutations of E-cadherin promoter were constructed. These plasmids were separately co-transfected with LMO2 into Lncap cells and the luciferase activity was detected after 24 h. Results： The overexpression of LMO2 could significantly inhibit the activity of luciferase reporter gene of E-cadherin promoter about 50%. Truncated and point mutation study showed that this was mainly through E-box sites in the promoter region -204/-198. Conclusion： The proto- oncngene LMO2 can affect the progression and metastasis mechanism of prostate cancer by transcriptional inhibition of E-cadherin.

关 键 词：LMO2 E-钙粘蛋白 前列腺癌 启动子 

分 类 号：R73-37[医药卫生—肿瘤]