Cytokine & growth factor reviews, 2002-02, Vol.13 (1), p.41-59
2002
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Details
- Autor(en) / Beteiligte
- Titel
- Role of the hepatocyte growth factor receptor, c-Met, in oncogenesis and potential for therapeutic inhibition
- Ist Teil von
- Cytokine & growth factor reviews, 2002-02, Vol.13 (1), p.41-59
- Ort / Verlag
- England: Elsevier Ltd
- Erscheinungsjahr
- 2002
- Quelle
- Elsevier Journal Backfiles on ScienceDirect (DFG Nationallizenzen)
- Beschreibungen/Notizen
- Receptor tyrosine kinases have become important therapeutic targets for anti-neoplastic molecularly targeted therapies. c-Met is a receptor tyrosine kinase shown to be over-expressed and mutated in a variety of malignancies. Stimulation of c-Met via its ligand hepatocyte growth factor also known as scatter factor (HGF/SF), leads to a plethora of biological and biochemical effects in the cell. There has been considerable knowledge gained on the role of c-Met–HGF/SF axis in normal and malignant cells. This review summarizes the structure of c-Met and HGF/SF and their family members. Since there are known mutations of c-Met in solid tumors, particularly in papillary renal cell carcinoma, we have summarized the various mutations and over-expression of c-Met known thus far. Stimulation of c-Met can lead to scattering, angiogenesis, proliferation, enhanced cell motility, invasion, and eventual metastasis. The biological functions altered by c-Met are quite unique and described in detail. Along with biological functions, various signal transduction pathways, including the cytoskeleton are altered with the activation of c-Met–HGF/SF loop. We have recently shown the phosphorylation of focal adhesion proteins, such as paxillin and p125FAK in response to c-Met stimulation in lung cancer cells, and this is detailed here. Finally, c-Met when mutated or over-expressed in malignant cells serves as an important therapeutic target and the most recent data in terms of inhibition of c-Met and downstream signal transduction pathways is summarized.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1359-6101DOI: 10.1016/S1359-6101(01)00029-6Titel-ID: cdi_proquest_miscellaneous_18303644
- Format
- –
- Schlagworte
- Amino Acid Sequence, Animals, Antineoplastic Agents - pharmacology, c-Met, c-Met protein, Cell Division, Cell motility and migration, Cell Movement, Hepatocyte Growth Factor - metabolism, Hepatocyte growth factor receptors, Hepatocyte growth factor/scatter factor, Humans, Inhibitors, Ligands, Metastasis, Models, Biological, Molecular Sequence Data, Mutation, Neoplasms - metabolism, Neoplasms - therapy, Neovascularization, Pathologic, paxillin, Phylogeny, Protein Binding, Proto-Oncogene Proteins c-met - physiology, Reactive Oxygen Species, scatter factor, Sequence Homology, Amino Acid, Signal transduction, Tumor Cells, Cultured