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

Hepatocyte growth factor suppresses the anticancer effect of irinotecan by decreasing the level of active metabolite in HepG2 cells

2011 ◽  
Vol 82 (11) ◽  
pp. 1720-1730 ◽  
Author(s):  
Manabu Okumura ◽  
Tomomi Iwakiri ◽  
Akinori Takagi ◽  
Yasutoshi Hirabara ◽  
Yohei Kawano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Active Metabolite ◽  
Anticancer Effect ◽  
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 Down-regulation of CMTM8 Induces Epithelial-to-Mesenchymal Transition-like Changes via c-MET/Extracellular Signal-regulated Kinase (ERK) Signaling

2012 ◽  
Vol 287 (15) ◽  
pp. 11850-11858 ◽  
Author(s):  
Wenjuan Zhang ◽  
Michelle C. Mendoza ◽  
Xiaolei Pei ◽  
Didem Ilter ◽  
Sarah J. Mahoney ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Tumor Cell ◽  
Hepg2 Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Mapk Pathway ◽  
Cellular Transformation ◽  
Down Regulation ◽  
Mesenchymal Transition ◽  
Hepatocyte Growth

The acquisition of an invasive phenotype is a critical turning point for malignant tumor cells. CMTM8, a potential tumor suppressor, is frequently down-regulated in solid tumors, and its overexpression induces tumor cell apoptosis. Here, we identify a new role for CMTM8 in regulating tumor cell migration. Reducing CMTM8 expression in HepG2 hepatocellular carcinoma cells results in the acquisition of epithelial-to-mesenchymal transition (EMT) features, including a morphological change from organized epithelial sheets to scattered fibroblast-like shapes, reduction of the epithelial marker E-cadherin, and an increased invasive and migratory ability. These phenotypic changes are mediated in large part by the ERK-MAPK pathway, as the MEK inhibitor U0126 and shRNA-mediated knockdown of ERK2 significantly reversed these phenotypes. Hepatocyte growth factor binding to the c-MET receptor is known to induce EMT in HepG2 cells. We found that CMTM8 knockdown in HepG2 cells induced c-MET signaling and ERK activation. Inhibition of c-MET signaling with the small molecule inhibitor SU11274 or c-MET RNAi blocked the EMT-like changes following CMTM8 knockdown. CMTM8 overexpression in HepG2 cells inhibited hepatocyte growth factor-induced EMT-like morphological changes and cell motility. Down-regulation of CMTM8 also promoted an EMT-like change in MCF-10A cells, indicating a broader role for CMTM8 in regulating cellular transformation.

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.

TRPV channels and modulation by hepatocyte growth factor/scatter factor in human hepatoblastoma (HepG2) cells

Cell Calcium ◽  
2004 ◽  
Vol 36 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Joris Vriens ◽  
Annelies Janssens ◽  
Jean Prenen ◽  
Bernd Nilius ◽  
Robert Wondergem
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Scatter Factor ◽  
Trpv Channels ◽  
Hepatocyte Growth
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