Journal
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
Volume 126, Issue 12, Pages 671-681Publisher
SPRINGER
DOI: 10.1007/s004320000143
Keywords
cell migration; metastasis formation; cell-matrix interaction; cytoskeleton; chemokine
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Increasing evidence has shown that the molecular regulation of active cell migration of slow-moving cells, e.g., tumor cells and fibroblasts, is different from fast-moving leukocytes, e.g., T lymphocytes and neutrophil granulocytes. Slow-moving cells develop focal adhesions as a crucial regulatory element during migration. These focal adhesions connect the extracellular matrix to the intracellular actin- and tubulin-cytoskeleton via integrins and enzymatically active proteins. Beside matrix-binding integrins, ligands of receptor tyrosine kinases and heterotrimeric G protein-coupled serpentine receptors initiate migration of slow-moving cells. Focal adhesions are not found in T lymphocytes and neutrophil granulocytes moving within three-dimensional matrices. In T lymphocytes, the T cell receptor is supposed to have a key regulatory function not only in antigen recognition, cell activation, and proliferation but also in cell migration. Regulatory molecules as well as the cytoskeleton are connected to the T cell receptor. The T cell receptor functionally combines elements of receptor tyrosine kinase signaling and of focal adhesions. In neutrophil granulocytes no multi-protein complexes regulating migration have been identified so far. Most potent activators of migration of neutrophil granulocytes, as those of T lymphocytes, are chemokines binding to heterotrimeric G protein-coupled serpentine receptors.
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