Abstract
The E-cadherin-beta-catenin complex plays a pivotal role in epithelial cell-cell adhesion and in the maintenance of differentiated adult epithelia. Perturbation of its expression or function is widely involved in tumor progression and metastasis. Recent years have seen a rapid expansion in the understanding of the biology and the clinical relevance of the E-cadherin adhesion complex in human lung cancer. During human lung cancer progression genomic, transcriptional and post-transcriptional alterations of the E-cadherin-beta-catenin adhesion system are implicated and comprise deletion of the chromosomic region 3p21 that comprise the locus of the gene encoding beta-catenin, transcriptional downregulation of E-cadherin, cytoplasmic redistribution, phosphorylation of both proteins and proteolysis of E-cadherin. E-cadherin-inactivating mutations and oncogenic-activating mutation of beta-catenin are not reported.
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