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A core function for p120-catenin in cadherin turnover.
Michael A Davis1, Renee C Ireton, Albert B Reynolds
1Department of Cancer Biology, Vanderbilt University, Nashville, TN 37232-6840, USA.
The Journal of Cell Biology
|November 12, 2003
Summary
p120-catenin controls cell adhesion by regulating cadherin levels at the cell surface. Loss of p120-catenin leads to decreased cadherin expression and impaired cell-cell adhesion, impacting tumor growth.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- p120-catenin is known to stabilize epithelial cadherin (E-cadherin).
- The precise mechanism by which p120-catenin influences E-cadherin stability and cell adhesion remains unclear.
Purpose of the Study:
- To elucidate the mechanism by which p120-catenin regulates cadherin levels and cell-cell adhesion.
- To investigate the role of p120-catenin in controlling cadherin turnover at the cell surface.
Main Methods:
- Utilized siRNA to knockdown p120-catenin expression in SW48 cells.
- Assessed the levels of various cadherins, including E-cadherin, placental cadherin, neuronal cadherin, and vascular endothelial cadherin.
- Evaluated the impact of p120-catenin knockdown on cell-cell adhesion.
Main Results:
- p120-catenin knockdown resulted in a dose-dependent decrease in multiple cadherin types.
- Complete loss of cell-cell adhesion was observed upon significant p120-catenin reduction.
- ARVCF and delta-catenin demonstrated functional redundancy, indicating a requirement for at least one p120 family member for adhesion.
Conclusions:
- p120-catenin plays a critical role at the cell surface in regulating cadherin turnover and maintaining cadherin levels.
- The findings suggest a direct correlation between p120-catenin levels and E-cadherin expression in tumors.
- Down-regulation of p120-catenin is predicted to lead to a loss of E-cadherin and impaired cell adhesion in cancer.