Migration inhibition of mammary epithelial cells by Syk is blocked in the presence of DDR1 receptors |
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| Authors: | Brit Neuhaus Sebastian Bühren Barbara Böck Frauke Alves Wolfgang F. Vogel Friedemann Kiefer |
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| Affiliation: | 1.Department of Vascular Cell Biology,Max Planck Institute for Molecular Biomedicine,Münster,Germany;2.Department of Hematology and Oncology,University Medical Center G?ttingen,G?ttingen,Germany;3.Department of Molecular Biology of Neuronal Signals,Max Planck Institute of Experimental Medicine,G?ttingen,Germany;4.Department of Laboratory Medicine and Pathobiology,University of Toronto,Toronto,Canada;5.Division of Vascular Oncology and Metastasis (A190),German Cancer Research Center (DKFZ),Heidelberg,Germany;6.Department of Biological Mechanisms of Ageing,Max Planck Institute for Biology of Ageing,Cologne,Germany |
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| Abstract: | The non-receptor tyrosine kinase Syk is a well-characterized hematopoietic signal transducer, which is also expressed in non-hematopoietic cells. In epithelial cells, the function of Syk is not wholly known. It interacts with the receptor tyrosine kinase DDR1 and is frequently lost from metastatic mammary tumors. Here, using genetic tracing, we demonstrate Syk expression in murine mammary epithelium, myoepithelium and skin epithelium, but not in intestinal or lung epithelia. Investigating possible functions of Syk, we found a substantial suppression of cell mobility that depended on Syk kinase activity in trans-well migration and wounding assays. Co-expression of DDR1 resulted in constitutive interaction and strong activation of Syk kinase. Most importantly, Syk-mediated migration inhibition was blocked in the presence of DDR1, while conversely DDR1 knockdown restored migration inhibition. Our study identifies Syk as a potent inhibitor of epithelial migration and describes a first functional consequence of the interaction with the collagen receptor DDR1. |
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