Epigenetic control of E-cadherin (CDH1) by CpG methylation in metastasising laryngeal cancer

被引:1
|
作者
Azarschab, P
Stembalska, A
Loncar, MB
Pfister, M
Sasiadek, M
Blin, N
机构
[1] Univ Tubingen, Div Mol Genet, Inst Anthropol & Human Genet, D-72074 Tubingen, Germany
[2] Univ Clin, Dept Otolaryngol, D-72076 Tubingen, Germany
[3] Wroclaw Med Univ, Dept Genet, PL-50368 Wroclaw, Poland
关键词
adhesion molecules; metastasis; gene inactivation; methylation;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Intercellular adhesion is promoted by many-fold structures formed by interacting molecules. One prominent protein family, called cadherins, consists of calcium-dependent proteins contributing to cell differentiation, migration and extracellular signal transduction. E-cadherin, regularly expressed in epithelial tissues, displays aberrant activity patterns in a variety of tumors. We have explored the mode of E-cadherin regulation in 98 biopsy samples from 76 patients with laryngeal carcinoma (80 primary tumors and 18 metastases). Transcriptional silencing of the gene (CDH1) achieved by promoter methylation was tested by a, methylation-specific PCR. In primary tumors, CDH1 methylation was noted in 40%. However, 77% of the tested metastases showed CDH1 methylation, 23% remained unmethylated (p<0.01). These data suggest that the E-cadherin promoter is subjected to epigenetic control connected with biological aggressiveness of laryngeal cancer in advanced steps of neoplastic transformation.
引用
收藏
页码:501 / 503
页数:3
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