HGF/SF-Met signaling in tumor progression
- 1 January 2005
- journal article
- review article
- Published by Springer Nature in Cell Research
- Vol. 15 (1) , 49-51
- https://doi.org/10.1038/sj.cr.7290264
Abstract
Tumor progression is a multi-step process that requires a sequential selection of specific malignant phenotypes. Met activation may induce different phenotypes depending on tumor stage: inducing proliferation and angiogenesis in primary tumors, stimulating motility to form micrometastases, and regaining the proliferation phenotype to form overt metastases. To study how HGF/SF-induced proliferative phenotypes switch to the invasive phenotype is important for understanding the mechanism of tumor progression and will provide an attractive target for cancer intervention and therapy.Keywords
This publication has 26 references indexed in Scilit:
- RNA Interference Reveals that Ligand-Independent Met Activity Is Required for Tumor Cell Signaling and SurvivalCancer Research, 2004
- Overexpression of sprouty 2 inhibits HGF/SF-mediated cell growth, invasion, migration, and cytokinesisOncogene, 2004
- Met, metastasis, motility and moreNature Reviews Molecular Cell Biology, 2003
- Rap1 GTPase Regulation of Adherens Junction Positioning and Cell AdhesionScience, 2002
- Requirement of Stat3 signaling for HGF/SF-Met mediated tumorigenesisOncogene, 2002
- Coupling Met to Specific Pathways Results in Distinct Developmental OutcomesMolecular Cell, 2001
- Src Homology 2-containing Inositol 5-Phosphatase 1 Binds to the Multifunctional Docking Site of c-Met and Potentiates Hepatocyte Growth Factor-induced Branching TubulogenesisJournal of Biological Chemistry, 2001
- A novel germ line juxtamembrane Met mutation in human gastric cancerOncogene, 2000
- Hepatocyte Growth Factor-induced Scatter of Madin-Darby Canine Kidney Cells Requires Phosphatidylinositol 3-KinaseJournal of Biological Chemistry, 1995
- Identification of the Hepatocyte Growth Factor Receptor As the c- met Proto-Oncogene ProductScience, 1991