PMID- 8612619
OWN - NLM
STAT- MEDLINE
DCOM- 19960603
LR  - 20211203
IS  - 0014-2956 (Print)
IS  - 0014-2956 (Linking)
VI  - 236
IP  - 2
DP  - 1996 Mar 1
TI  - Dissociation of c-fos induction and mitogen-activated-protein kinase activation 
      from the hepatocyte-growth-factor-induced motility response in human gastric 
      carcinoma cells.
PG  - 476-81
AB  - The function of hepatocyte growth factor/scatter factor (HGF/SF) is to increase 
      proliferation as well as to stimulate motility and disperse cell colonies of 
      epithelial cells. In this study, we examined the motogenic and mitogenic 
      responses of two human gastric carcinoma cell types, MKN7 and MKN74. Cell 
      motility of both cell lines was markedly stimulated by HGF/SF. In contrast, 
      HGF/SF stimulated cell growth of MKN74 cells, but did not stimulate growth of 
      MKN7 cells. To address the cause of the difference in response of these cells, 
      which may reflect some differences in signaling pathways downstream from the 
      HGF/SF receptor, c-Met, we investigated the induction of the proto-oncogene 
      c-fos. The level of c-fos mRNA increased and reached a maximum approximately 40 
      min after HGF/SF stimulation in MKN74 cells, and thereafter its level rapidly 
      decreased. In contrast, the level of c-fos expression was very low irrespective 
      of the stimulation in MKN7 cells. c-Fos protein was transiently induced only in 
      MKN74 cells l h after treatment with HGF/SF, and its levels subsequently 
      decreased. We subsequently examined the activation of mitogen-activated-protein 
      kinase, which is a major mediator in the signaling pathway leading to the 
      stimulation of c-fos transcription, after HGF/SF treatment in both cell lines. 
      Mitogen-activated-protein kinase was markedly activated by this treatment in 
      MKN74 cells, but was only slightly activated in MKN7 cells. These results suggest 
      that although mitogen-activated-protein kinase activation and c-fos induction 
      play an essential role in the signaling pathway leading to cell growth, they are 
      not required for the motility response induced by HGF/SF.
FAU - Nagamine, K
AU  - Nagamine K
AD  - Department of Biochemistry, Faculty of Pharmaceutical Sciences, Setsunan 
      University, Japan.
FAU - Shibamoto, S
AU  - Shibamoto S
FAU - Takeuchi, K
AU  - Takeuchi K
FAU - Miyazawa, K
AU  - Miyazawa K
FAU - Kitamura, N
AU  - Kitamura N
FAU - Chatani, Y
AU  - Chatani Y
FAU - Kohno, M
AU  - Kohno M
FAU - Ito, F
AU  - Ito F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Eur J Biochem
JT  - European journal of biochemistry
JID - 0107600
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (MAS1 protein, human)
RN  - 0 (Oligodeoxyribonucleotides)
RN  - 0 (Proto-Oncogene Mas)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
SB  - IM
MH  - Adenocarcinoma/*physiopathology
MH  - Base Sequence
MH  - Calcium-Calmodulin-Dependent Protein Kinases/*metabolism
MH  - Cell Division/drug effects
MH  - Cell Movement/drug effects
MH  - DNA-Binding Proteins/metabolism
MH  - Enzyme Activation
MH  - Hepatocyte Growth Factor/*physiology
MH  - Humans
MH  - Molecular Sequence Data
MH  - Oligodeoxyribonucleotides/chemistry
MH  - Proto-Oncogene Mas
MH  - Proto-Oncogene Proteins c-fos/*physiology
MH  - Signal Transduction
MH  - Stomach Neoplasms/*physiopathology
MH  - Tumor Cells, Cultured
EDAT- 1996/03/01 00:00
MHDA- 1996/03/01 00:01
CRDT- 1996/03/01 00:00
PHST- 1996/03/01 00:00 [pubmed]
PHST- 1996/03/01 00:01 [medline]
PHST- 1996/03/01 00:00 [entrez]
AID - 10.1111/j.1432-1033.1996.t01-1-00476.x [doi]
PST - ppublish
SO  - Eur J Biochem. 1996 Mar 1;236(2):476-81. doi: 
      10.1111/j.1432-1033.1996.t01-1-00476.x.