Effect of hepatocyte growth factor on methionine adenosyltransferase genes and growth is cell density-dependent in HepG2 cells

2006 ◽  
Vol 210 (3) ◽  
pp. 766-773 ◽  
Author(s):  
Heping Yang ◽  
Nathaniel Magilnick ◽  
Mazen Noureddin ◽  
José M. Mato ◽  
Shelly C. Lu
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Density ◽  
Hepg2 Cells ◽  
Methionine Adenosyltransferase ◽  
Density Dependent ◽  
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 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 Sequential Activation of ERK and Repression of JNK by Scatter Factor/Hepatocyte Growth Factor in Madin-Darby Canine Kidney Epithelial Cells

2000 ◽  
Vol 11 (11) ◽  
pp. 3751-3763 ◽  
Author(s):  
Réjane Paumelle ◽  
David Tulasne ◽  
Catherine Leroy ◽  
Jean Coll ◽  
Bernard Vandenbunder ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Cell Density ◽  
Transcriptional Response ◽  
Madin Darby Canine Kidney ◽  
Scatter Factor ◽  
Hepatocyte Growth ◽  
Darby Canine Kidney ◽  
Canine Kidney

The scattering of Madin-Darby canine kidney (MDCK) epithelial cells by scatter factor/hepatocyte growth factor (SF/HGF) is associated with transcriptional induction of the urokinase gene, which occurs essentially through activation of an EBS/AP1 response element. We have investigated the signal transduction pathways leading to this transcriptional response. We found that SF/HGF induces rapid and sustained phosphorylation of the extracellular signal-regulated kinase (ERK) MAPK while stimulating weakly and then repressing phosphorylation of the JUN N-terminal kinase (JNK) MAPK for several hours. This delayed repression of JNK was preceded by phosphorylation of the MKP2 phosphatase, and both MKP2 induction and JNK dephosphorylation were under the control of MEK, the upstream kinase of ERK. ERK and MKP2 stimulate the EBS/AP1-dependent transcriptional response to SF/HGF, but not JNK, which inhibits this response. We further demonstrated that depending on cell density, the RAS-ERK-MKP2 pathway controls this transrepressing effect of JNK. Together, these data demonstrate that in a sequential manner SF/HGF activates ERK and MKP2, which in turn dephosphorylates JNK. This sequence of events provides a model for efficient cell scattering by SF/HGF at low cell density.

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.

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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