Bussemakers M J, Giroldi L A, van Bokhoven A, Schalken J A
Urology Research Laboratory, University Hospital Nijmegen, The Netherlands.
Biochem Biophys Res Commun. 1994 Sep 15;203(2):1284-90. doi: 10.1006/bbrc.1994.2321.
Decreased expression of the Ca(2+)-dependent cell adhesion molecule E-cadherin is observed in several poorly differentiated carcinomas and is presumably associated with an invasive phenotype of these tumors. Evidence accumulated so far indicates that decreased transcription is a major mechanism leading to defective E-cadherin function. Therefore, we isolated and characterized the human E-cadherin gene promoter and studied the transcriptional regulation of this gene in two human prostate cancer cell lines, one expressing E-cadherin (PC-3), the other one not expressing E-cadherin (TSU-pr1). We show that the E-cadherin promoter is not active in the non-expressing cells and that this may be due to the binding of a repressor protein to the promoter.
在几种低分化癌中观察到钙依赖性细胞粘附分子E-钙粘蛋白的表达降低,推测这与这些肿瘤的侵袭性表型有关。迄今为止积累的证据表明,转录减少是导致E-钙粘蛋白功能缺陷的主要机制。因此,我们分离并鉴定了人E-钙粘蛋白基因启动子,并在两个人前列腺癌细胞系中研究了该基因的转录调控,其中一个表达E-钙粘蛋白(PC-3),另一个不表达E-钙粘蛋白(TSU-pr1)。我们发现E-钙粘蛋白启动子在不表达的细胞中无活性,这可能是由于一种阻遏蛋白与启动子结合所致。