作者: Roger Abounader , John Laterra
DOI: 10.1215/S1152851705000050
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摘要: The multifunctional growth factor scatter factor/hepatocyte (SF/HGF) and its receptor tyrosine kinase c-Met have emerged as key determinants of brain tumor angiogenesis. SF/HGF are expressed in tumors, the expression levels frequently correlating with grade, blood vessel density, poor prognosis. Overexpression and/or cells enhances their tumorigenicity, growth, tumor-associated Conversely, inhibition experimental xenografts leads to is secreted mainly by acts on receptors that vascular endothelial cells. Activation induction proliferation, migration, invasion apoptosis well also induces extracellular matrix degradation, tubule formation, angiogenesis vivo. directly through only partly known mechanisms indirectly regulating other angiogenic pathways such VEGF. Different approaches inhibiting been recently developed. These include antagonism fragments NK4, SF/HGF, U1snRNA/ribozymes; competitive ligand binding soluble Met receptors; neutralizing antibodies SF/HGF; small molecular inhibitors. Use these inhibitors models In this review, we summarize current knowledge how SF/HGF:c-Met pathway contributes malignancy a focus glioma