c‐erbB‐2/EGFR as dominant heterodimerization partners determine a motogenic phenotype in human breast cancer cells

• DOI: 10.1096/fasebj.13.14.1939
• Publication Date: 2018-01-25T09:39:04Z
• Authors: Burkhard H. Brandt; Antje Roetger; Thomas Dittmar; Gerd Nikolai; Matthes Seeling; Anja Merschjann; Jerzy‐Roch Nofer; Gunda Dehmer‐Möller; Ralf Junker; Gerd Assmann; Kurt S. Zaenker
• Keywords: ErbB; Cell Signaling

Separate mechanisms for oncogenesis and metastasis have been postulated. We show here that prolonged invasive cell migration, a key mechanism in cancer metastasis, is linked to c-erbB-2 signaling. Cell lines with EGFR expression transphosphorylation activity display high transendothelial invasiveness an endothelial-extra-cellular matrix model mimicking capillary vessel wall vitro. Tyrosine-phosphorylated receptors are localized predominantly areas of the membrane extension activity. On molecular level, there subtle cross talk between transmembrane signaling molecule actin cytoskeleton at multiple levels, including generation second messenger PIP2 mobilization actin-regulatory protein gelsolin. Our data strongly suggest c-erbB-2, especially heterodimer EGFR, closely involved pathways, inducing alterations morphology required human breast become motile conceivably metastatic.—Brandt, B. H., Roetger, A., Dittmar, T., Nikolai, G., Seeling, M., Merschjann, Nofer, J.-R., Dehmer-Möller, Junker, R., Assmann, Zaenker. K. S. c-erbB-2/EGFR as dominant heterodimerization partners determine motogenic phenotype cells. FASEB J. 13, 1939–1949 (1999)