scholarly journals Gelsolin-mediated activation of PI3K/Akt pathway is crucial for hepatocyte growth factor-induced cell scattering in gastric carcinoma

Oncotarget ◽  
2016 ◽  
Vol 7 (18) ◽  
pp. 25391-25407 ◽  
Author(s):  
Baohua Huang ◽  
Shuo Deng ◽  
Ser Yue Loo ◽  
Arpita Datta ◽  
Yan Lin Yap ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gastric Carcinoma ◽  
Hepatocyte Growth Factor ◽  
Akt Pathway ◽  
Cell Scattering ◽  
Hepatocyte Growth

scholarly journals Enhancement of Hepatocyte Growth Factor-Induced Cell Scattering in N-Acetylglucosaminyltransferase III-transfected HepG2 Cells

2004 ◽  
Vol 27 (6) ◽  
pp. 781-785 ◽  
Author(s):  
Masashi Hyuga ◽  
Sumiko Hyuga ◽  
Nana Kawasaki ◽  
Miyako Ohta ◽  
Satsuki Itoh ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Cell Scattering ◽  
Hepatocyte Growth

scholarly journals Hepatocyte growth factor induces cell scattering through MAPK/Egr-1-mediated upregulation of Snail

2006 ◽  
Vol 25 (15) ◽  
pp. 3534-3545 ◽  
Author(s):  
Stefan Grotegut ◽  
Dietrich von Schweinitz ◽  
Gerhard Christofori ◽  
François Lehembre
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Scattering ◽  
Hepatocyte Growth

scholarly journals Modulation of E-Cadherin by Hepatocyte Growth Factor Induces Aggressiveness of Gastric Carcinoma

2005 ◽  
Vol 242 (5) ◽  
pp. 676-683 ◽  
Author(s):  
Sang-Uk Han ◽  
Hwa-Young Lee ◽  
Jae-Ho Lee ◽  
Wook-Hwan Kim ◽  
Hyunja Nam ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gastric Carcinoma ◽  
Hepatocyte Growth Factor ◽  
Hepatocyte Growth ◽  
E Cadherin

scholarly journals Hepatocyte Growth Factor Attenuates Transforming Growth Factor-β-Angiotensin II Crosstalk Through Inhibition of the PTEN/Akt Pathway

Hypertension ◽  
2011 ◽  
Vol 58 (2) ◽  
pp. 190-196 ◽  
Author(s):  
Kazuma Iekushi ◽  
Yoshiaki Taniyama ◽  
Hiroshi Kusunoki ◽  
Junya Azuma ◽  
Fumihiro Sanada ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Akt Pathway ◽  
Hepatocyte Growth

scholarly journals Hepatocyte Growth Factor stimulated cell scattering requires ERK and Cdc42-dependent tight junction disassembly

2010 ◽  
Vol 400 (2) ◽  
pp. 271-277 ◽  
Author(s):  
Akashi Togawa ◽  
Jeffery Sfakianos ◽  
Shuta Ishibe ◽  
Sayuri Suzuki ◽  
Yoshihide Fujigaki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Tight Junction ◽  
Cell Scattering ◽  
Hepatocyte Growth

scholarly journals Kruppel-like factor 4 is involved in cell scattering induced by hepatocyte growth factor

2012 ◽  
Vol 125 (20) ◽  
pp. 4853-4864 ◽  
Author(s):  
J.-K. Lai ◽  
H.-C. Wu ◽  
Y.-C. Shen ◽  
H.-Y. Hsieh ◽  
S.-Y. Yang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Scattering ◽  
Hepatocyte Growth

scholarly journals Activation of Both MAP Kinase and Phosphatidylinositide 3-Kinase by Ras Is Required for Hepatocyte Growth Factor/Scatter Factor–induced Adherens Junction Disassembly

1998 ◽  
Vol 9 (8) ◽  
pp. 2185-2200 ◽  
Author(s):  
Sandra Potempa ◽  
Anne J. Ridley
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Map Kinase ◽  
Adherens Junctions ◽  
Adherens Junction ◽  
Dominant Negative ◽  
Cell Junctions ◽  
Scatter Factor ◽  
Cell Scattering ◽  
Hepatocyte Growth

Hepatocyte growth factor/scatter factor (HGF/SF) stimulates the motility of epithelial cells, initially inducing centrifugal spreading of colonies followed by disruption of cell–cell junctions and subsequent cell scattering. In Madin–Darby canine kidney cells, HGF/SF-induced motility involves actin reorganization mediated by Ras, but whether Ras and downstream signals regulate the breakdown of intercellular adhesions has not been established. Both HGF/SF and V12Ras induced the loss of the adherens junction proteins E-cadherin and β-catenin from intercellular junctions during cell spreading, and the HGF/SF response was blocked by dominant-negative N17Ras. Desmosomes and tight junctions were regulated separately from adherens junctions, because they were not disrupted by V12Ras. MAP kinase, phosphatidylinositide 3-kinase (PI 3-kinase), and Rac were required downstream of Ras, because loss of adherens junctions was blocked by the inhibitors PD098059 and LY294002 or by dominant-inhibitory mutants of MAP kinase kinase 1 or Rac1. All of these inhibitors also prevented HGF/SF-induced cell scattering. Interestingly, activated Raf or the activated p110α subunit of PI 3-kinase alone did not induce disruption of adherens junctions. These results indicate that activation of both MAP kinase and PI 3-kinase by Ras is required for adherens junction disassembly and that this is essential for the motile response to HGF/SF.

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