Expression of hepatocyte growth factor/scatter factor, its activator, inhibitors and the c-Met receptor in human cancer cells

2001 ◽  
Author(s):  
Christian Parr ◽  
Wen Jiang
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cancer Cells ◽  
Human Cancer ◽  
Met Receptor ◽  
Scatter Factor ◽  
Human Cancer Cells ◽  
Hepatocyte Growth

Involvement of hepatocyte growth factor/scatter factor and Met receptor signaling in hair follicle morphogenesis and cycling

2000 ◽  
Vol 14 (2) ◽  
pp. 319-332 ◽  
Author(s):  
Gerd Lindner ◽  
Andreas Menrad ◽  
Ermanno Gherardi ◽  
Glenn Merlino ◽  
Pia Welker ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hair Follicle ◽  
Receptor Signaling ◽  
Met Receptor ◽  
Scatter Factor ◽  
Hepatocyte Growth

scholarly journals Scatter factor and hepatocyte growth factor are indistinguishable ligands for the MET receptor.

1991 ◽  
Vol 10 (10) ◽  
pp. 2867-2878 ◽  
Author(s):  
L. Naldini ◽  
K.M. Weidner ◽  
E. Vigna ◽  
G. Gaudino ◽  
A. Bardelli ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Met Receptor ◽  
Scatter Factor ◽  
Hepatocyte Growth

scholarly journals Hepatocyte Growth Factor/Scatter Factor Blocks the Mitochondrial Pathway of Apoptosis Signaling in Breast Cancer Cells

2001 ◽  
Vol 276 (50) ◽  
pp. 47257-47265 ◽  
Author(s):  
Min Gao ◽  
Saijun Fan ◽  
Itzhak D. Goldberg ◽  
John Laterra ◽  
Richard N. Kitsis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Fas Ligand ◽  
Parp Cleavage ◽  
Scatter Factor ◽  
Mitochondrial Membrane Depolarization ◽  
Hepatocyte Growth

The cytokine hepatocyte growth factor/scatter factor (HGF/SF) has been found to protect a variety of epithelial and cancer cell types against cytotoxicity and apoptosis induced by DNA damage, but the specific apoptotic signaling events and the levels at which they are blocked by HGF/SF have not been identified. We found that treatment of MDA-MB-453 human breast cancer cells with adriamycin (also known as doxorubicin, a DNA topoisomerase IIα inhibitor) induced a series of time-dependent events, including the mitochondrial release of cytochromecand apoptosis-inducing factor, mitochondrial membrane depolarization, activation of a set of caspases (caspase-9, -3, -7, -2, and -8), cleavage of poly(ADP-ribose) polymerase (PARP), and up-regulation of expression of the Fas ligand. All of these events were blocked by preincubation of the cells with HGF/SF. In contrast, the pan-caspase inhibitor benzyloxycarbonyl-VAD-fluoromethylketone blocked some of these events (e.g.caspase-3 activation and PARP cleavage) but did not block cytochromecrelease or mitochondrial depolarization. These findings suggest that HGF/SF functions, in part, upstream of the mitochondria to block mitochondrial apoptosis signaling, prevent activation of multiple caspases, and protect breast cancer cells against apoptosis.

scholarly journals The Met receptor tyrosine kinase transduces motility, proliferation, and morphogenic signals of scatter factor/hepatocyte growth factor in epithelial cells.

1993 ◽  
Vol 121 (1) ◽  
pp. 145-154 ◽  
Author(s):  
K M Weidner ◽  
M Sachs ◽  
W Birchmeier
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Tyrosine Kinase ◽  
Cell Motility ◽  
Receptor Tyrosine Kinase ◽  
Met Receptor ◽  
Scatter Factor ◽  
Met Receptor Tyrosine Kinase ◽  
Hepatocyte Growth

Depending on the target cells and culture conditions, scatter factor/hepatocyte growth factor (SF/HGF) mediates several distinct activities, i.e., cell motility, proliferation, invasiveness, tubular morphogenesis, angiogenesis, or cytotoxicity. A small isoform of SF/HGF encoded by a natural splice variant, which consists of the NH2-terminal hairpin structure and the first two kringle domains but not the protease homology region, induces cell motility but not mitogenesis. Two types of SF/HGF receptors have recently been discovered in epithelial cells, the high affinity c-Met receptor tyrosine kinase, and low affinity/high capacity binding sites, which are probably located on heparan sulfate proteoglycans. In the present study, we have addressed the question whether the various biological activities of SF/HGF are transduced into cells by a single type of receptor. We have here examined MDCK epithelial cells transfected with a hybrid cDNA encoding the ligand binding domain of the nerve growth factor (NGF) receptor and the membrane-spanning and tyrosine kinase domains of the Met receptor. We demonstrate that all biological effects of SF/HGF upon epithelial cells such as the induction of cell motility, proliferation, invasiveness, and tubular morphogenesis can now be triggered by the addition of NGF. Thus, it is likely that all known biological signals of SF/HGF are transduced through the receptor tyrosine kinase encoded by the c-Met protooncogene.

Expression of c-Met receptor and hepatocyte growth factor/scatter factor in synovial sarcoma and epithelioid sarcoma

1998 ◽  
Vol 432 (4) ◽  
pp. 337-342 ◽  
Author(s):  
C. Kuhnen ◽  
Edina Tolnay ◽  
Hans Ulrich Steinau ◽  
Bruno Voss ◽  
Klaus-Michael Müller
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Synovial Sarcoma ◽  
Epithelioid Sarcoma ◽  
Met Receptor ◽  
Scatter Factor ◽  
Hepatocyte Growth

Hepatocyte growth factor / scatter factor and m-MET receptor expression during murine anagen development

1998 ◽  
Vol 16 ◽  
pp. S151
Author(s):  
Gerd Lindner ◽  
Andreas Menrad ◽  
Pia Welker ◽  
Sven Mueller-Roever ◽  
Ralf Paus
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Receptor Expression ◽  
Met Receptor ◽  
Scatter Factor ◽  
Hepatocyte Growth
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