2002
DOI: 10.1172/jci200215429
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The cadherin-catenin adhesion system in signaling and cancer

Abstract: The adhesion of cells to their neighbors determines cellular and tissue morphogenesis and regulates major cellular processes including motility, growth, differentiation, and survival. Cell-cell adherens junctions (AJs), the most common (indeed, essentially ubiquitous) type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. AJs assemble via homophilic interactions between the extracellular domains of calcium-dependent ca… Show more

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Cited by 244 publications
(329 citation statements)
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“…OVCAR3 cells were treated once with 20 mM NAC, and Caco-2 cells were treated once with 10 mM NAC structure in colon carcinoma cells and of the cornified envelope in keratinocytes; (iii) the basal relocation of the nucleus in Caco-2 cells together with the formation of a robust apical vesicular apparatus; (iv) an overall rearrangement of cytoskeleton to fulfill the requirements of newly formed structures; (v) the appearance of several cell-cell and cellsubstratum junctions; and, finally, (vi) the disappearance of the oncogenic b-catenin from the nucleus and its only presence at the cell-cell junctions. Taken together, the relocation of b-catenin at the level of junctions and the increased concentration of E-cadherin represent both markers and inducers of differentiation [22][23][24][25][26] suggesting the establishment of a positive feedback in the differentiation process. The increase in cell-cell and cell-substratum adhesions identifies a more adhesive and less motile phenotype.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…OVCAR3 cells were treated once with 20 mM NAC, and Caco-2 cells were treated once with 10 mM NAC structure in colon carcinoma cells and of the cornified envelope in keratinocytes; (iii) the basal relocation of the nucleus in Caco-2 cells together with the formation of a robust apical vesicular apparatus; (iv) an overall rearrangement of cytoskeleton to fulfill the requirements of newly formed structures; (v) the appearance of several cell-cell and cellsubstratum junctions; and, finally, (vi) the disappearance of the oncogenic b-catenin from the nucleus and its only presence at the cell-cell junctions. Taken together, the relocation of b-catenin at the level of junctions and the increased concentration of E-cadherin represent both markers and inducers of differentiation [22][23][24][25][26] suggesting the establishment of a positive feedback in the differentiation process. The increase in cell-cell and cell-substratum adhesions identifies a more adhesive and less motile phenotype.…”
Section: Discussionmentioning
confidence: 99%
“…24,25,37 Among other functions related to the proliferation/differentiation transition, the nonreceptor tyrosine kinase c-Src has a pivotal role in b-catenin relocation. 38,39 Robust in vitro evidences bind the modulation of c-Src kinase activity to the redox state of a group of four cysteine residues close to its catalytic site, a key target for a mutually counteracting reversible control operated by oxidizing and reducing agents.…”
Section: Discussionmentioning
confidence: 99%
“…[21][22][23] The accumulation of cytoplasmic b-catenin and its translocation to the nucleus has been associated with epithelial cell migration and invasion in various physiological and pathological processes including tumour progression. 21,[23][24][25][26] Several b-catenin/TCF target genes have now been identified. They pertain to various families of proteins including matrix metalloproteases, cytoskeletal proteins or angiogenic cytokines and chemokines (IL-8, MMP-7, MMP-14, CD44, cyclin D1, c-myc, claudin-1, vimentin, MMP26, VEGF.…”
mentioning
confidence: 99%
“…Cadherins comprise a family of transmembrane cell surface glycoproteins that mediate calcium (Ca 2 þ )-dependent, homotypic cell -cell interactions through their extracellular domains, and regulate a variety of biological processes during development, morphogenesis, and tumour metastasis (Gumbiner, 1996;Yap et al, 1997;Conacci-Sorrell et al, 2002). Ca 2 þ -dependent cell -cell adhesion usually consists of rapid localisation of surface Ecadherin molecules to the regions of contact, resulting in homotypic binding that fosters the maintenance of normal cellular structure.…”
mentioning
confidence: 99%
“…As carcinomas progress to the invasive and metastatic stages, select adhesive epithelial cells usually undergo a mesenchymal-like transition that enables their movement from the primary tumour mass (Comoglio and Boccaccio, 2001;Conacci-Sorrell et al, 2002). During this process in breast, gastric, and pancreatic metastatic carcinomas, E-cadherin expression is frequently downregulated or even undetectable Lowy et al, 2002).…”
mentioning
confidence: 99%