| HGF/SF-met signaling may up-regulate oncogenes, signal transduction genes, apoptosis-related genes, metastasis related genes, and down-regulate a number of genes. | unknown |
| Hepatocyte growth factor(HGF/SF)facilitates intercellular communication between the epithelial carcinoma and surrounding stromal tissue during metastatic invasion through interaction with its proto-oncogenic receptor, Met, found on carcinoma cells. | liver |
| Mimp expression reduces hepatocyte growth factor/scatter factor-induced proliferation and scattering by attenuating and altering the downstream signaling of met proto-oncogene. | liver |
| the relatively infrequent expression of HGF and Met in Wilms_ tumor tumorigenesis reflects their roles in nephrogenesis, particularly the mesenchymal-to-epithelial transition, rather than a dependence on oncogenic signaling pathways. | Wilms |
| Studies suggest that although serum proto-oncogene proteins c-met (MET) and hepatocyte growth factor (HGF) may serve as predictive biomarkers for MET therapeutics, data do not support their use as pharmacodynamic biomarkers for onartuzumab. | liver |
| Data show that monoclonal antibody ARGX-111 inhibits hepatocyte growth factor (HGF)-dependent proto-oncogene protein c-met (MET) activity by competing with HGF for binding to MET. | liver |
| The findings suggest that the oncogenic activity of hepsin arises not only from elevated expression level but also from depletion of HAI-1, events which together trigger gain-of-function activity impacting HGF/MET signalling and epithelial cohesion | unknown |
| MiR-7 was upregulated in MCF-10A cells by hepatocyte growth factor (HGF), and subsequently downregulated upon treatment with siRNA against HGF. HGF expression did not significantly change through either an upregulation or downregulation of miR-7 expression, suggesting that HGF acts upstream of miR-7. Results indicate that miR-7 mediates the activity of HGF to suppress oncogenic proteins. | liver |