Transformation of cell adhesion properties by exogenously introduced E-cadherin cDNA

Nature ◽  
1987 ◽  
Vol 329 (6137) ◽  
pp. 341-343 ◽  
Author(s):  
Akira Nagafuchi ◽  
Yasuaki Shirayoshi ◽  
Kenji Okazaki ◽  
Kunio Yasuda ◽  
Masatoshi Takeichi
Keyword(s):  
Cell Adhesion ◽  
Adhesion Properties ◽  
E Cadherin

scholarly journals Microgravity Induces Transient EMT in Human Keratinocytes by Early Down-Regulation of E-Cadherin and Cell-Adhesion Remodeling

2020 ◽  
Vol 11 (1) ◽  
pp. 110
Author(s):  
Giulia Ricci ◽  
Alessandra Cucina ◽  
Sara Proietti ◽  
Simona Dinicola ◽  
Francesca Ferranti ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Human Keratinocytes ◽  
Short Exposure ◽  
Migration And Invasion ◽  
Hacat Cells ◽  
Invasive Phenotype ◽  
Adhesion Properties ◽  
Mesenchymal Transition ◽  
Cell Matrix ◽  
E Cadherin

Changes in cell–matrix and cell-to-cell adhesion patterns are dramatically fostered by the microgravity exposure of living cells. The modification of adhesion properties could promote the emergence of a migrating and invasive phenotype. We previously demonstrated that short exposure to the simulated microgravity of human keratinocytes (HaCaT) promotes an early epithelial–mesenchymal transition (EMT). Herein, we developed this investigation to verify if the cells maintain the acquired invasive phenotype after an extended period of weightlessness exposure. We also evaluated cells’ capability in recovering epithelial characteristics when seeded again into a normal gravitational field after short microgravity exposure. We evaluated the ultra-structural junctional features of HaCaT cells by Transmission Electron Microscopy and the distribution pattern of vinculin and E-cadherin by confocal microscopy, observing a rearrangement in cell–cell and cell–matrix interactions. These results are mirrored by data provided by migration and invasion biological assay. Overall, our studies demonstrate that after extended periods of microgravity, HaCaT cells recover an epithelial phenotype by re-establishing E-cadherin-based junctions and cytoskeleton remodeling, both being instrumental in promoting a mesenchymal–epithelial transition (MET). Those findings suggest that cytoskeletal changes noticed during the first weightlessness period have a transitory character, given that they are later reversed and followed by adaptive modifications through which cells miss the acquired mesenchymal phenotype.

scholarly journals Dynamics of Cell Interactions and Communications during Melanoma Development

2002 ◽  
Vol 13 (1) ◽  
pp. 62-70 ◽  
Author(s):  
G. Li ◽  
K. Satyamoorthy ◽  
M. Herlyn
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Intercellular Communication ◽  
Cell Adhesion Molecules ◽  
Cell Interactions ◽  
Adhesion Properties ◽  
Environmental Controls ◽  
And Migration ◽  
E Cadherin ◽  
Cell Cell

Melanoma development not only involves genetic and epigenetic changes that take place within the cell, but also involves processes determined collectively by micro-environmental factors, including cell-cell interactions and communications. During the transition from normal cells to benign and malignant lesions, and subsequently to metastatic cancer, stepwise changes in intercellular communications provide tumor cells with the ability to overcome cell-cell adhesion and micro-environmental controls from the host and to invade surrounding tissues and disperse to distant locations. Cadherins are major cell–cell adhesion molecules involved in the development and maintenance of skin. E-cadherin expressed in normal melanocytes mediates growth and invasion control by keratinocytes. Progressive loss of E-cadherin and gain of N-cadherin during melanoma development not only free melanoma cells from control by keratinocytes, but also provide new adhesion properties, resulting in switched partnerships with fibroblasts and vascular endothelial cells. The cadherin subtype switching also dictates gap junctional specificity in melanocytic cells during tumor development. This selective intercellular communication may contribute to the regulation of cell growth, differentiation, apoptosis, and migration of melanocytic cells in both physiologic and pathologic conditions. Abnormal up-regulation of the immunoglobin repeat-containing cell adhesion molecules Mel-CAM and L1-CAM potentiates invasion and migration of melanoma. Thus, abnormal expression of intercellular adhesion receptors and dysregulated intercellular communication underlies melanoma development and progression.

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

scholarly journals T cell adhesion and cytolysis of pancreatic cancer cells: a role for E-cadherin in immunotherapy?

2002 ◽  
Vol 87 (9) ◽  
pp. 1034-1041 ◽  
Author(s):  
J J French ◽  
J Cresswell ◽  
W K Wong ◽  
K Seymour ◽  
R M Charnley ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Adhesion ◽  
T Cell ◽  
Cancer Cells ◽  
Pancreatic Cancer Cells ◽  
E Cadherin ◽  
T Cell Adhesion

scholarly journals Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells

2021 ◽  
Vol 15 (1) ◽  
pp. 1-17
Author(s):  
Sarah Alsharif ◽  
Pooja Sharma ◽  
Karina Bursch ◽  
Rachel Milliken ◽  
Van Lam ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cell Surface ◽  
Mcf7 Cells ◽  
Keratin 19 ◽  
E Cadherin ◽  
Cell Cell

Redistribution and dysfunction of integrins in cultured renal epithelial cells exposed to oxidative stress

1993 ◽  
Vol 264 (1) ◽  
pp. F149-F157 ◽  
Author(s):  
J. Gailit ◽  
D. Colflesh ◽  
I. Rabiner ◽  
J. Simone ◽  
M. S. Goligorsky
Keyword(s):  
Oxidative Stress ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Apical Cell ◽  
Flow Cytometric Analysis ◽  
Adhesion Properties ◽  
Renal Tubular Cells ◽  
Renal Tubular

Tubular obstruction by detached renal tubular epithelial cells is a major cause of oliguria in acute renal failure. Viable renal tubular cells can be recovered from urine of patients with acute tubular necrosis, suggesting a possible defect in cell adhesion to the basement membrane. To study this process of epithelial cell desquamation in vitro, we investigated the effect of nonlethal oxidative stress on the integrin adhesion receptors of the primate kidney epithelial cell line BS-C-1. Morphological and functional studies of cell adhesion properties included the following: interference reflection microscopy, intravital confocal microscopy and immunocytochemistry, flow cytometric analysis of integrin receptor abundance, and cell-matrix attachment assay. High levels of the integrin subunits alpha 3, alpha v, and beta 1 were detected on the cell surface by fluorescence-activated cell sorting (FACS) analysis, as well as lower levels of alpha 1, alpha 2, alpha 4, alpha 5, alpha 6, and beta 3. Exposure of BS-C-1 cells to nonlethal oxidative stress resulted in the disruption of focal contacts, disappearance of talin from the basal cell surface, and in the redistribution of integrin alpha 3-subunits from predominantly basal location to the apical cell surface. As measured in a quantitative cell attachment assay, oxidative stress decreased BS-C-1 cell adhesion to type IV collagen, laminin, fibronectin, and vitronectin. Defective adhesion was not associated with a loss of alpha 3-, alpha 4-, or alpha v-integrin subunits from the cell surface.(ABSTRACT TRUNCATED AT 250 WORDS)

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