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The two-handed E box binding zinc finger protein SIP1 downregulates E-cadherin and induces invasion.
It is reported that expression of wild-type but not of mutated SIP1 downregulates mammalian E-cadherin transcription via binding to both conserved E2 boxes of the minimal E- cadheringin promoter.
Release of an invasion promoter E-cadherin fragment by matrilysin and stromelysin-1.
The results suggest a novel mechanism by which metalloproteinases can influence invasion, as indicated by induction of invasion into collagen type I and inhibition of E-cadherin-dependent cell aggregation.
Loss of epithelial differentiation and gain of invasiveness correlates with tyrosine phosphorylation of the E-cadherin/beta-catenin complex in cells transformed with a temperature-sensitive v-SRC gene
A mechanism by which v-src counteracts junctional assembly and thereby promotes invasiveness and dedifferentiation of epithelial cells through phosphorylation of the E-cadherin/catenin complex is suggested.
Genetic manipulation of E-cadherin expression by epithelial tumor cells reveals an invasion suppressor role
Evidence is provided that E-cadherin acts as an invasion suppressor molecule in epithelial tumor cell lines of dog kidney or mouse mammary gland origin.
Clinical, cellular, and molecular aspects of cancer invasion.
The molecular analysis of invasion-associated cellular activities, namely, homotypic and heterotypic cell-cell adhesion, cell-matrix interactions and ectopic survival, migration, and proteolysis, reveal branching signal transduction pathways with extensive networks between individual pathways.
Dissecting tumor cell invasion: epithelial cells acquire invasive properties after the loss of uvomorulin-mediated cell-cell adhesion
It is shown that nontransformed Madin-Darby canine kidney epithelial cells acquire invasive properties when intercellular adhesion is specifically inhibited by the addition of antibodies against the cell adhesion molecule uvomorulin; the separated cells then invade collagen gels and embryonal heart tissue.
Implication of the MAGI‐1b/PTEN signalosome in stabilization of adherens junctions and suppression of invasiveness
It is proposed that the recruitment of PTEN at adherens junctions by MAGI‐1b and the local down‐regulation of phosphatidylinositol‐3,4,5‐trisphosphate pools and downstream effector systems at the site of cell‐cell contacts are focal points for restraining both disruption of junctional complexes and induction of tumor cell invasion.
Leptin promotes invasiveness of kidney and colonic epithelial cells via phosphoinositide 3‐kinase‐, Rho‐, and Rac‐dependent signaling pathways
It is indicated that leptin may exert a local and beneficial effect on migration of normal colonic epithelial cells and reparation of the inflamed or wounded digestive mucosa, linking the nutritional and body fat status to digestive cancer susceptibility by stimulating the invasive capacity of colonichelial cells at early stages of neoplasia.
E‐cadherin/catenin/cytoskeleton complex: A regulator of cancer invasion
Mechanisms of Invasion and Metastasis
This work focuses on the role of Tumor-Host Components as Elements of Malignancy in Invasion and Metastasis, and the roles of Hydrolases and Cell-Cell Adhesion Molecules in Malignancies.