Induction of polarized cell-cell association and retardation of growth by activation of the E-cadherin-catenin adhesion system in a dispersed carcinoma line.
Open accessAbstract
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 alpha-catenin, a cadherin-associated protein. However, when the E-cadherin is activated by transfection with alpha-catenin cDNA, they form spherical aggregates, each consisting of an enclosed monolayer cell sheet. In the present work, we examined whether the alpha-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 alpha-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.
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E-cadherin is a key determinant of junctional polarity in both simple and stratified epithelia.
“For example, E-cadherin is a key determinant of junctional polarity in both simple and stratified epithelia9, 34”
From E-cadherin integrates mechanotransduction and EGFR signaling to control junctional tissue polarization and tight junction positioning (2017) · cites this paper as [9]
The paper reports that activating E-cadherin in PC9 carcinoma cells triggered a polarized junctional complex characteristic of simple epithelia (p. 247), supporting that part of the claim. It does not establish the same role in stratified epithelia, so the claim extends beyond the setting studied. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn vitro studies have shown that E-cadherin is necessary for adherens junction formation and its adhesive activity is crucial for assembly of desmosomes, gap junctions and tight junctions.
“In vitro studies have shown that E-cadherin is not only necessary for adherens junction formation but its adhesive activity is also crucial for the assembly of other junctional complexes such as desmosomes, gap junctions and tight junctions (Gumbiner et al, 1988;Musil et al, 1990;Watabe et al, 1994).”
From E‐cadherin is essential for in vivo epidermal barrier function by regulating tight junctions (2005) · cites this paper as Watabe et al, 1994
The study reports that activating E-cadherin in PC9 cells produced adherens junctions, tight junctions and desmosomes (p. 247), and its Discussion calls cadherin-mediated contact a prerequisite for forming the latter two (pp. 252–253). But it does not show that E-cadherin's adhesive activity is crucial for gap-junction assembly: the Introduction (p. 247) only says that introducing a cadherin into cadherin-deficient cells enhances gap-junction formation. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn vitro studies using mostly simple epithelial cells have indicated that E-cadherin-mediated adhesion is a necessary prerequisite for the formation of other cell junctions, such as desmosomes, gap junctions and tight junctions.
“In vitro studies using mostly simple epithelial cells have indicated that E-cadherin-mediated adhesion is a necessary prerequisite for the formation of other cell junctions, such as desmosomes, gap junctions and tight junctions (Gumbiner et al, 1988;Musil et al, 1990;Watabe et al, 1994).”
From E‐cadherin is essential for in vivo epidermal barrier function by regulating tight junctions (2005) · cites this paper as Watabe et al, 1994
The Introduction (pp. 247–248) describes cadherins as prerequisites for epithelial junctional complexes, and the Discussion (p. 252) presents evidence that E-cadherin-mediated contact precedes tight-junction and desmosome formation. For gap junctions, however, the paper says cadherin introduction enhances their formation; it does not establish E-cadherin-mediated adhesion as necessary for them. (LLM, conf=0.84)
Experimental — accuracy not yet measuredStudies in lower organisms and mammalian cell cultures have identified a central role for E-cadherin in coordinating the establishment of apico-basolateral polarity with the formation of AJs, desmosomes, and TJs.
“Studies in lower organisms and mammalian cell cultures have identified a central role for E-cadherin in coordinating the establishment of apico–basolateral polarity with the formation of AJs, desmosomes, and TJs1, 9.”
From E-cadherin integrates mechanotransduction and EGFR signaling to control junctional tissue polarization and tight junction positioning (2017) · cites this paper as [9]
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Guo, X., Rao, J. N., Liu, L., Zou, T.-T., Turner, D. J., Bass, B. L., & Wang, J.-Y. (2003) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00015.2003 · Cited by 153 · see citing works
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- Authors
- Watabe, M., Nagafuchi, A., Tsukita, S., & Takeichi, M.
- Affiliations
- Kyoto University (JP)
- ORCID
- Takeichi, M
- Venue
- The Journal of cell biology
- Publisher
- Rockefeller University Press
- Published
- 1994-10-01
- Volume
- 127
- Issue
- 1
- Pages
- 247-256
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2120192
- OpenAlex
- W2106104738
- Cited by
- 399
- References
- 0
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 7 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 5 · 2019: 5 · 2018: 9 · 2017: 6 · 2016: 5 · 2015: 8 · 2014: 9 · 2013: 11 · 2012: 11
- FWCI
- 7.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- E-cadherin, alpha-catenin, cell-cell adhesion, epithelial polarity, ZO-1, tight junctions, adherens junctions, desmosomes, cell aggregation, epithelial phenotype
- MeSH terms
- Cell Adhesion, Cell Division, Cytoskeletal Proteins, Epithelial Cells, Humans, Intercellular Junctions, Laminin, Membrane Proteins, Phenotype, Phosphoproteins, Transfection, Tumor Cells, Cultured, Cell Adhesion Molecules, Cadherins, Integrins, Cell Polarity, DNA, Complementary, alpha Catenin, Zonula Occludens-1 Protein
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