1. E-cadherin Surface Levels in Epithelial Growth Factor-stimulated Cells Depend on Adherens Junction Protein Shrew-1
- Author
-
Knut Engels, Julia Christina Gross, Anna Starzinski-Powitz, and Alexander Schreiner
- Subjects
Receptor, ErbB-2 ,medicine.medical_treatment ,media_common.quotation_subject ,Green Fluorescent Proteins ,Immunoblotting ,Fluorescent Antibody Technique ,Breast Neoplasms ,Biology ,Adherens junction ,Cell Movement ,Epidermal growth factor ,Cell Line, Tumor ,medicine ,Humans ,Mammary Glands, Human ,Internalization ,Molecular Biology ,media_common ,Microscopy, Confocal ,Epidermal Growth Factor ,Reverse Transcriptase Polymerase Chain Reaction ,Cell adhesion molecule ,Cadherin ,Growth factor ,Adherens Junctions ,Articles ,Cell Biology ,Cadherins ,Endocytosis ,Cell biology ,ErbB Receptors ,src-Family Kinases ,Cell culture ,RNA Interference ,Signal transduction ,Cell Adhesion Molecules ,Signal Transduction - Abstract
Gain- and loss-of-function studies indicate that the adherens junction protein shrew-1 acts as a novel modulator of E-cadherin internalization induced by epithelial growth factor (EGF) or E-cadherin function-blocking antibody during epithelial cell dynamics. Knocking down shrew-1 in MCF-7 carcinoma cells preserves E-cadherin surface levels upon EGF stimulation. Overexpression of shrew-1 leads to preformation of an E-cadherin/EGF receptor (EGFR) HER2/src-kinase/shrew-1 signaling complex and accelerated E-cadherin internalization. Shrew-1 is not sufficient to stimulate E-cadherin internalization, but facilitates the actions of EGFR and thus may promote malignant progression in breast cancer cells with constitutive EGFR stimulation by reducing surface E-cadherin expression.
- Published
- 2009