PMID- 9524768
OWN - NLM
STAT- MEDLINE
DCOM- 19980518
LR  - 20190905
IS  - 0300-5208 (Print)
IS  - 0300-5208 (Linking)
VI  - 212
DP  - 1997
TI  - Scatter factor receptors are key players in a unique multistep program leading to 
      invasive growth.
PG  - 133-44; discussion 144-7
AB  - Hepatocyte growth factor/scatter factor (HGF/SF) is the prototype of a family of 
      structurally related soluble molecules (scatter factors) which also includes the 
      HGF-like/macrophage-stimulating protein (HGF1/MSP). HGF/SF and HGF1/MSP control a 
      complex genetic program known as 'invasive growth' which leads to cell 
      dissociation, proliferation, invasion of extracellular matrix, prevention of 
      apoptosis, acquisition of polarity and tubule formation. The HGF/SF and HGF1/MSP 
      receptors are the tyrosine kinases encoded by the homologous genes met and ron. 
      During development coordinated control of invasive growth by HGF-Met is 
      essential. Met and Ron receptor signalling occurs via a two-phosphotyrosine 
      multifunctional docking site located in their C-terminal regions. Activation of 
      Ras and phosphatidylinositol-3-kinase through the multifunctional docking site is 
      required for receptor-mediated invasive growth. In a number of malignant tumours 
      met and ron are mutated, amplified or overexpressed. Oncogenically activated met 
      and ron confer transforming, invasive and metastatic properties to normal cells. 
      Point mutations of the multifunctional docking site dissociate the transforming 
      potential from the invasive-metastatic phenotype showing that distinct signalling 
      pathways are involved. This review summarizes the recent progress made in 
      understanding the signalling mechanisms initiated by the scatter factor receptors 
      leading to invasive growth.
FAU - Bardelli, A
AU  - Bardelli A
AD  - Institute for Cancer Research (IRCC), University of Torino Medical School, Italy.
FAU - Comoglio, P M
AU  - Comoglio PM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Ciba Found Symp
JT  - Ciba Foundation symposium
JID - 0356636
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
RN  - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
SB  - IM
MH  - Animals
MH  - Cell Division/physiology
MH  - Cell Polarity/physiology
MH  - Cell Survival/physiology
MH  - Humans
MH  - Mice
MH  - Neoplasm Invasiveness
MH  - Neoplasms/pathology/*physiopathology
MH  - Proto-Oncogene Proteins c-met/genetics/*physiology
MH  - Signal Transduction/physiology
MH  - Urokinase-Type Plasminogen Activator/metabolism
RF  - 64
EDAT- 1997/01/01 00:00
MHDA- 1998/04/03 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1998/04/03 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - 10.1002/9780470515457.ch9 [doi]
PST - ppublish
SO  - Ciba Found Symp. 1997;212:133-44; discussion 144-7. doi: 
      10.1002/9780470515457.ch9.