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The Role of the E-Cadherin/Catenin Adhesion Complex in the Development and Progression of Cancer

https://doi.org/10.1006/mcbr.1999.0155Get rights and content

Abstract

The E-cadherin/catenin protein complex regulates the functional integrity of epithelia by mediating specific intercellular adhesion. Defects in the transmembrane E-cadherin protein play an important role in several human cancer types. E-cadherin-inactivating mutations were mainly found in sporadic lobular breast carcinoma and in both familial and sporadic diffuse gastric carcinoma. Armadillo proteins such as β-catenin and p120ctn are complexed to the cytoplasmic tail of E-cadherin, whereas the vinculin-related αE-catenin protein forms a link to the actin cytoskeleton. The latter shows inactivating deletions in various tumor cell lines. Apparently, both E-cadherin and αE-catenin serve as tumor suppressor and invasion suppressor molecules. On the other hand, protein-stabilizing oncogenic mutations of β-catenin were found at high frequency in particular human tumor types. Mutated β-catenin protein is imported into the nucleus, and its binding to LEF/TCF transcription factors modulates transcription of intriguing target genes. Also p120ctn was recently found to arrive in the nucleus and to interact with a transcription factor. Furthermore, a wide variety of mechanisms have been described to regulate in a reversible way E-cadherin/catenin-mediated cell adhesion and differentiation. These phenomena appear to be crucial in human cancer development and progression.

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