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Cadherin/catenin complex: A target for antiinvasive therapy?
Author(s) -
Mareel Marc,
Berx Geert,
Roy Frans Van,
Bracke Marc
Publication year - 1996
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19960616)61:4<524::aid-jcb5>3.0.co;2-q
Subject(s) - downregulation and upregulation , cadherin , phosphorylation , catenin , biology , microbiology and biotechnology , signal transduction , tyrosine phosphorylation , extracellular , transmembrane protein , cell adhesion , cancer research , cell adhesion molecule , receptor , gene , wnt signaling pathway , cell , genetics
Invasion is a major challenge for cancer therapy. Invasion or noninvasion results from the cross talk between cancer cells and host cells, building molecular invasion‐promoter and invasion‐suppressor complexes. The E‐cadherin/catenin invasion‐suppressor complex is attractive as a target for a putative antiinvasive therapy because of its multifactorial regulation at multiple levels and sometimes in a reversible way. Mutations in the E‐cadherin gene combined with loss of the wild type allele causes irreversible downregulation in some human cancers. Posttranslational and reversible downregulation may occur by tyrosine phosphorylation of β‐catenin. Phosphorylation is implicated also in transmembrane receptor signal transduction through the E‐cadherin/catenin complex. Homophilic interaction with E‐cadherin on another cell through a dimeric adhesion zipper, involving the HAV sequence of the first extracellular domains, is the major extracellular link of the E‐cadherin/catenin complex. Intracellularly, the list of proteins that bind to or signal through the complex or one or more of its elements is growing. In vitro, insulin‐like growth factor‐I, and tamoxifen may upregulate the functions of the E‐cadherin/catenin complex and inhibit invasion, demonstrating that this complex may serve as a target for antiinvasive therapy. © 1996 Wiley‐Liss, Inc.