Induction of Polarized Cell-Cell Association and Retardation of Growth by Activation of the E-Cadherin-Catenin Adhesion System in a Dispersed Carcinoma Line

PC9 lung carcinoma cells cannot tightly associate with one another, and therefore grow singly, despite their expression of E-cadherin, because of their lack of α-catenin, a cadherin-associated protein. However, when the E-cadherin is activated by transfection with α-catenin cDNA, they form spherical...

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Bibliographic Details
Published in:The Journal of cell biology 1994-10, Vol.127 (1), p.247-256
Main Authors: Watabe, Mitsuko, Nagafuchi, Akira, Tsukita, Sachiko, Takeichi, Masatoshi
Format: Article
Language:English
Subjects:
alpha Catenin
Antibodies
Cadherins
Cadherins - analysis
Cell Adhesion
Cell Adhesion Molecules - analysis
Cell aggregates
Cell Division
Cell growth
Cell lines
Cell Polarity - physiology
Cells
Cellular biology
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - physiology
DNA, Complementary
Epithelial Cells
Humans
Integrins - analysis
Intercellular Junctions - chemistry
Intercellular Junctions - ultrastructure
Laminin
Lung cancer
Membrane Proteins - analysis
Molecules
Phenotype
Phosphoproteins - analysis
Proteins
Tight junctions
Transfection
Tumor Cells, Cultured
Zonula Occludens-1 Protein
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Summary:PC9 lung carcinoma cells cannot tightly associate with one another, and therefore grow singly, despite their expression of E-cadherin, because of their lack of α-catenin, a cadherin-associated protein. However, when the E-cadherin is activated by transfection with α-catenin cDNA, they form spherical aggregates, each consisting of an enclosed monolayer cell sheet. In the present work, we examined whether the α-catenin-transfected cell layers expressed epithelial phenotypes, by determining the distribution of various cell adhesion molecules on their surfaces, including E-cadherin, ZO-1, desmoplakin, integrins, and laminin. In untransfected PC9 cells, all these molecules were randomly distributed on their cell surface. In the transfected cells, however, each of them was redistributed into a characteristic polarized pattern without a change in the amount of expression. Electron microscopic study demonstrated that the α-catenin-transfected cell layers acquired apical-basal polarity typical of simple epithelia; they formed microvilli only on the outer surface of the aggregates, and a junctional complex composed of tight junction, adherens junction, and desmosome arranged in this order. These results indicate that the activation of E-cadherin triggered the formation of the junctional complex and the polarized distribution of cell surface proteins and structures. We also found that, in untransfected PC9 cells, ZO-1 formed condensed clusters and colocalized with E-cadherin, but that other adhesion molecules rarely showed such colocalization with E-cadherin, suggesting that there is some specific interaction between ZO-1 and E-cadherin even in the absence of cell-cell contacts. In addition, we found that the activation of E-cadherin caused a retardation of PC9 cell growth. Thus, we concluded that the E-cadherin-catenin adhesion system is essential not only for structural organization of epithelial cells but also for the control of their growth.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.127.1.247