HGF/SF-Met signaling in tumor progression

Cell Res. 2005 Jan;15(1):49-51. doi: 10.1038/sj.cr.7290264.


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.

Publication types

  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • Cell Proliferation
  • Disease Progression*
  • GRB2 Adaptor Protein
  • Hepatocyte Growth Factor / metabolism*
  • Humans
  • Inositol Polyphosphate 5-Phosphatases
  • Models, Biological
  • Neoplasm Metastasis
  • Neoplasms / metabolism
  • Neoplasms / pathology*
  • Neovascularization, Pathologic
  • Phenotype
  • Phosphoric Monoester Hydrolases / metabolism
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-cbl
  • Proto-Oncogene Proteins c-met / metabolism*
  • Signal Transduction*
  • Ubiquitin-Protein Ligases / metabolism
  • ras Proteins / metabolism


  • Adaptor Proteins, Signal Transducing
  • GRB2 Adaptor Protein
  • GRB2 protein, human
  • Proto-Oncogene Proteins
  • Hepatocyte Growth Factor
  • Proto-Oncogene Proteins c-cbl
  • Ubiquitin-Protein Ligases
  • Proto-Oncogene Proteins c-met
  • Phosphoric Monoester Hydrolases
  • Inositol Polyphosphate 5-Phosphatases
  • ras Proteins