A Core Function for p120-Catenin in Cadherin Turnover

p120-catenin stabilizes epithelial cadherin (E-cadherin) in SW48 cells, but the mechanism has not been established. Here, we show that p120 acts at the cell surface to control cadherin turnover, thereby regulating cadherin levels. p120 knockdown by siRNA expression resulted in dose-dependent elimina...

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Bibliographic Details
Published in:The Journal of cell biology 2003-11, Vol.163 (3), p.525-534
Main Authors: Davis, Michael A., Ireton, Renee C., Reynolds, Albert B.
Format: Article
Language:English
Subjects:
Adherens Junctions - genetics
Adherens Junctions - metabolism
Armadillo Domain Proteins
Cadherins
Cadherins - genetics
Cadherins - metabolism
Catenins
Cell adhesion
Cell Adhesion - physiology
Cell Adhesion Molecules - antagonists & inhibitors
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - metabolism
Cell Line, Tumor
Cell lines
Cell Membrane - metabolism
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Cells
Cellular biology
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - metabolism
Down-Regulation - genetics
Epithelial cells
Gene expression regulation
Humans
Mice
Models, Biological
Neoplasms - genetics
Neoplasms - metabolism
Phosphoproteins - antagonists & inhibitors
Phosphoproteins - genetics
Phosphoproteins - metabolism
Ribonucleic acid
RNA
RNA, Small Interfering - pharmacology
Small interfering RNA
Tumors
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Summary:p120-catenin stabilizes epithelial cadherin (E-cadherin) in SW48 cells, but the mechanism has not been established. Here, we show that p120 acts at the cell surface to control cadherin turnover, thereby regulating cadherin levels. p120 knockdown by siRNA expression resulted in dose-dependent elimination of epithelial, placental, neuronal, and vascular endothelial cadherins, and complete loss of cell-cell adhesion. ARVCF and δ-catenin were functionally redundant, suggesting that proper cadherin-dependent adhesion requires the presence of at least one p120 family member. The data reveal a core function of p120 in cadherin complexes, and strongly predict a dose-dependent loss of E-cadherin in tumors that partially or completely down-regulate p120.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.200307111