scholarly journals Rack1 promotes epithelial cell–cell adhesion by regulating E-cadherin endocytosis

Oncogene ◽  
2011 ◽  
Vol 31 (3) ◽  
pp. 376-389 ◽  
Author(s):  
G Swaminathan ◽  
C A Cartwright
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
E Cadherin ◽  
Cell Cell

scholarly journals A molecular mechanism directly linking E-cadherin adhesion to initiation of epithelial cell surface polarity

2007 ◽  
Vol 178 (2) ◽  
pp. 323-335 ◽  
Author(s):  
Lene N. Nejsum ◽  
W. James Nelson
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
Cell Surface ◽  
Basolateral Membrane ◽  
Surface Polarity ◽  
Cell Contacts ◽  
Protein Receptors ◽  
Epithelial Cell Surface ◽  
E Cadherin ◽  
Cell Cell

Mechanisms involved in maintaining plasma membrane domains in fully polarized epithelial cells are known, but when and how directed protein sorting and trafficking occur to initiate cell surface polarity are not. We tested whether establishment of the basolateral membrane domain and E-cadherin–mediated epithelial cell–cell adhesion are mechanistically linked. We show that the basolateral membrane aquaporin (AQP)-3, but not the equivalent apical membrane AQP5, is delivered in post-Golgi structures directly to forming cell–cell contacts where it co-accumulates precisely with E-cadherin. Functional disruption of individual components of a putative lateral targeting patch (e.g., microtubules, the exocyst, and soluble N-ethylmaleimide–sensitive factor attachment protein receptors) did not inhibit cell–cell adhesion or colocalization of the other components with E-cadherin, but each blocked AQP3 delivery to forming cell–cell contacts. Thus, components of the lateral targeting patch localize independently of each other to cell–cell contacts but collectively function as a holocomplex to specify basolateral vesicle delivery to nascent cell–cell contacts and immediately initiate cell surface polarity.

scholarly journals CD151 regulates epithelial cell–cell adhesion through PKC- and Cdc42-dependent actin cytoskeletal reorganization

2003 ◽  
Vol 163 (1) ◽  
pp. 165-176 ◽  
Author(s):  
Masaki Shigeta ◽  
Noriko Sanzen ◽  
Masayuki Ozawa ◽  
Jianguo Gu ◽  
Hitoshi Hasegawa ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
Cytoskeletal Reorganization ◽  
Cortical Actin ◽  
A431 Cells ◽  
Kinase C ◽  
Integrin Α3β1 ◽  
E Cadherin ◽  
Cell Cell

CD151, a member of the tetraspanin family proteins, tightly associates with integrin α3β1 and localizes at basolateral surfaces of epithelial cells. We found that overexpression of CD151 in A431 cells accelerated intercellular adhesion, whereas treatment of cells with anti-CD151 mAb perturbed the integrity of cortical actin filaments and cell polarity. E-Cadherin puncta formation, indicative of filopodia-based adhesion zipper formation, as well as E-cadherin anchorage to detergent-insoluble cytoskeletal matrix, was enhanced in CD151-overexpressing cells. Levels of GTP-bound Cdc42 and Rac were also elevated in CD151-overexpressing cells, suggesting the role of CD151 in E-cadherin–mediated cell–cell adhesion as a modulator of actin cytoskeletal reorganization. Consistent with this possibility, engagement of CD151 by the substrate-adsorbed anti-CD151 mAb induced prominent Cdc42-dependent filopodial extension, which along with E-cadherin puncta formation, was strongly inhibited by calphostin C, a protein kinase C (PKC) inhibitor. Together, these results indicate that CD151 is involved in epithelial cell–cell adhesion as a modulator of PKC- and Cdc42-dependent actin cytoskeletal reorganization.

scholarly journals Plasticity in epithelial cell phenotype: modulation by expression of different cadherin cell adhesion molecules.

1995 ◽  
Vol 129 (2) ◽  
pp. 507-519 ◽  
Author(s):  
J A Marrs ◽  
C Andersson-Fisone ◽  
M C Jeong ◽  
L Cohen-Gould ◽  
C Zurzolo ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
Apical Membrane ◽  
Retinal Pigment ◽  
Cell Phenotype ◽  
Cell Contacts ◽  
Membrane Cytoskeleton ◽  
E Cadherin ◽  
Cell Cell

A primary function of cadherins is to regulate cell adhesion. Here, we demonstrate a broader function of cadherins in the differentiation of specialized epithelial cell phenotypes. In situ, the rat retinal pigment epithelium (RPE) forms cell-cell contacts within its monolayer, and at the apical membrane with the neural retina; Na+, K(+)-ATPase and the membrane cytoskeleton are restricted to the apical membrane. In vitro, RPE cells (RPE-J cell line) express an endogenous cadherin, form adherens junctions and a tight monolayer, but Na+,K(+)-ATPase is localized to both apical and basal-lateral membranes. Expression of E-cadherin in RPE-J cells results in restriction and accumulation of both Na+,K(+)-ATPase and the membrane cytoskeleton at the lateral membrane; these changes correlate with the synthesis of a different ankyrin isoform. In contrast to both RPE in situ and RPE-J cells that do not form desmosomes, E-cadherin expression in RPE-J cells induces accumulation of desmoglein mRNA, and assembly of desmosome-keratin complexes at cell-cell contacts. These results demonstrate that cadherins directly affect epithelial cell phenotype by remodeling the distributions of constitutively expressed proteins and by induced accumulation of specific proteins, which together lead to the generation of structurally and functionally distinct epithelial cell types.

scholarly journals ADAM10 mediates E-cadherin shedding and regulates epithelial cell-cell adhesion, migration, and  -catenin translocation

2005 ◽  
Vol 102 (26) ◽  
pp. 9182-9187 ◽  
Author(s):  
T. Maretzky ◽  
K. Reiss ◽  
A. Ludwig ◽  
J. Buchholz ◽  
F. Scholz ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
E Cadherin ◽  
Cell Cell

scholarly journals Spatial and temporal dissection of immediate and early events following cadherin-mediated epithelial cell adhesion.

1993 ◽  
Vol 120 (5) ◽  
pp. 1217-1226 ◽  
Author(s):  
H McNeill ◽  
T A Ryan ◽  
S J Smith ◽  
W J Nelson
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
Cell Structure ◽  
Cell Contact ◽  
Differential Interference Contrast Microscopy ◽  
Rapid Acquisition ◽  
Lag Period ◽  
Triton X ◽  
E Cadherin ◽  
Cell Cell

Cell-cell adhesion is at the top of a molecular cascade of protein interactions that leads to the remodeling of epithelial cell structure and function. The earliest events that initiate this cascade are poorly understood. Using high resolution differential interference contrast microscopy and retrospective immunohistochemistry, we observed that cell-cell contact in MDCK epithelial cells consists of distinct stages that correlate with specific changes in the interaction of E-cadherin with the cytoskeleton. We show that formation of a stable contact is preceded by numerous, transient contacts. During this time and immediately following formation of a stable contact, there are no detectable changes in the distribution, relative amount, or Triton X-100 insolubility of E-cadherin at the contact. After a lag period of approximately 10 min, there is a rapid acquisition of Triton X-100 insolubility of E-cadherin localized to the stable contact. Significantly, the total amount of E-cadherin at the contact remains unchanged during this time. The increase in the Triton X-100 insoluble pool of E-cadherin does not correlate with changes in the distribution of actin or fodrin, suggesting that the acquisition of the Triton X-100 insolubility is due to changes in E-cadherin itself, or closely associated proteins such as the catenins. The 10 minute lag period, and subsequent prompt and localized nature of E-cadherin reorganization indicate a form of signaling is occurring.

scholarly journals Expression of N-cadherin by human squamous carcinoma cells induces a scattered fibroblastic phenotype with disrupted cell-cell adhesion.

1996 ◽  
Vol 135 (6) ◽  
pp. 1643-1654 ◽  
Author(s):  
S Islam ◽  
T E Carey ◽  
G T Wolf ◽  
M J Wheelock ◽  
K R Johnson
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Squamous Cell ◽  
Epithelial Cell Line ◽  
Squamous Epithelial Cell ◽  
Squamous Carcinoma Cells ◽  
E Cadherin ◽  
Cell Cell

E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic cell-cell adhesion and plays an important role in maintaining the normal phenotype of epithelial cells. Disruption of E-cadherin activity in epithelial cells correlates with formation of metastatic tumors. Decreased adhesive function may be implemented in a number of ways including: (a) decreased expression of E-cadherin; (b) mutations in the gene encoding E-cadherin; or (c) mutations in the genes that encode the catenins, proteins that link the cadherins to the cytoskeleton and are essential for cadherin mediated cell-cell adhesion. In this study, we explored the possibility that inappropriate expression of a nonepithelial cadherin by an epithelial cell might also result in disruption of cell-cell adhesion. We showed that a squamous cell carcinoma-derived cell line expressed N-cadherin and displayed a scattered fibroblastic phenotype along with decreased expression of E- and P-cadherin. Transfection of this cell line with antisense N-cadherin resulted in reversion to a normal-appearing squamous epithelial cell with increased E- and P-cadherin expression. In addition, transfection of a normal-appearing squamous epithelial cell line with N-cadherin resulted in downregulation of both E- and P-cadherin and a scattered fibroblastic phenotype. In all cases, the levels of expression of N-cadherin and E-cadherin were inversely related to one another. In addition, we showed that some squamous cell carcinomas expressed N-cadherin in situ and those tumors expressing N-cadherin were invasive. These studies led us to propose a novel mechanism for tumorigenesis in squamous epithelial cells; i.e., inadvertent expression of a nonepithelial cadherin.

scholarly journals Tuning Epithelial Cell–Cell Adhesion and Collective Dynamics with Functional DNA-E-Cadherin Hybrid Linkers

Nano Letters ◽  
2021 ◽  
Author(s):  
Andreas Schoenit ◽  
Cristina Lo Giudice ◽  
Nina Hahnen ◽  
Dirk Ollech ◽  
Kevin Jahnke ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cell ◽  
Collective Dynamics ◽  
Functional Dna ◽  
E Cadherin ◽  
Cell Cell

622: Von Hippel-Lindau Inactivation Downregulates the Cell-Cell Adhesion Molecule E Cadherin in Renal Cancer Cells

2005 ◽  
Vol 173 (4S) ◽  
pp. 170-170
Author(s):  
Maxine G. Tran ◽  
Miguel A. Esteban ◽  
Peter D. Hill ◽  
Ashish Chandra ◽  
Tim S. O'Brien ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cancer Cells ◽  
Renal Cancer ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Von Hippel Lindau ◽  
E Cadherin ◽  
Cell Cell
Sign in / Sign up

Export Citation Format

Share Document