From Tpr-Met to Met, tumorigenesis and tubes

Oncogene. 2007 Feb 26;26(9):1276-85. doi: 10.1038/sj.onc.1210201.


The receptor for hepatocyte growth factor (HGF)/scatter factor (SF), Met, controls a program of invasive epithelial growth through the coordination of cell proliferation and survival, cell migration and epithelial morphogenesis. This process is important during embryogenesis and for organ regeneration in the adult. However, when deregulated the HGF/SF-Met signaling axis contributes to tumorigenesis and metastasis. Studies on the oncogenic activation of the Met receptor have shed light on the molecular mechanisms underlying the oncogenic activation of receptor tyrosine kinase (RTKs). More than a decade ago, work on the Met related oncogene, Tpr-Met, revealed the mechanism for activation of RTK-derived oncogenes generated following chromosomal translocation. More recently, studies on the mechanisms of downregulation of the Met RTK highlight a role for loss of downregulation in RTK oncogenic activation.

Publication types

  • Review

MeSH terms

  • Cell Transformation, Neoplastic / genetics*
  • Hepatocyte Growth Factor / physiology
  • Humans
  • Neoplasm Invasiveness
  • Neoplasms / pathology
  • Nuclear Pore Complex Proteins / physiology*
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-met
  • Receptors, Growth Factor / physiology*
  • Signal Transduction
  • Ubiquitin / metabolism


  • Nuclear Pore Complex Proteins
  • Proto-Oncogene Proteins
  • Receptors, Growth Factor
  • TPR protein, human
  • Ubiquitin
  • Hepatocyte Growth Factor
  • MET protein, human
  • Proto-Oncogene Proteins c-met