PMID- 15365247
OWN - NLM
STAT- MEDLINE
DCOM- 20050209
LR  - 20131121
IS  - 1226-3613 (Print)
IS  - 1226-3613 (Linking)
VI  - 36
IP  - 4
DP  - 2004 Aug 31
TI  - Transforming variant of Met receptor confers serum independence and 
      anti-apoptotic property and could be involved in the mouse thymic 
      lymphomagenesis.
PG  - 283-91
AB  - Met tyrosine kinase receptor, the receptor of hepatocyte growth factor/scatter 
      factor (HGF/SF), is present in mouse tissues as two major isoforms differing by a 
      47-aminoacid segment in the juxtamembrane domain via alternative splicing of exon 
      14. We found that the smaller isoform of Met (Sm-Met) was highly transformable in 
      both in vitro and in vivo tumorigenesis assays. In this report, close examination 
      of the transforming activity of the Sm-Met showed that the expression of Sm-Met 
      conferred the cells serum independence and anti- apoptotic property when treated 
      with doxorubicin. These properties of Sm-Met seemed to be originated from its far 
      longer maintenance of tyrosine kinase activity after the binding of HGF/SF. 
      Interestingly, the longer maintenance of activated status was accompanied with 
      more increase of tyrosine phosphorylation of Stat3 protein. Moreover, we have 
      tried to find (an) animal tumorigenesis model(s) showing the increase in the 
      expression of this transforming variant of Met. In gamma-ray-induced mouse thymic 
      lymphoma model, the expression of the mRNAs for Sm-Met was significantly 
      increased as well as those of wild type Met and HGF/SF, suggesting a possible 
      role of the Sm-Met in tumorigenesis in vivo.
FAU - Baek, Cheol-Min
AU  - Baek CM
AD  - Department of Biochemistry, Ajou University Medical School, San 5 Woncheon-dong, 
      Yeongtong-gu, Suwon, 443-721, Korea.
FAU - Jeon, Soung-Hoo
AU  - Jeon SH
FAU - Jang, Ja-June
AU  - Jang JJ
FAU - Lee, Bok Soon
AU  - Lee BS
FAU - Lee, Jae-Ho
AU  - Lee JH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Exp Mol Med
JT  - Experimental & molecular medicine
JID - 9607880
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (Stat3 protein, mouse)
RN  - 0 (Trans-Activators)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - 80168379AG (Doxorubicin)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Cell Proliferation
MH  - Cell Survival
MH  - *Cell Transformation, Neoplastic
MH  - DNA-Binding Proteins/metabolism
MH  - Doxorubicin/pharmacology
MH  - Hepatocyte Growth Factor/pharmacology
MH  - Lymphoma/*etiology/genetics/metabolism
MH  - Mice
MH  - NIH 3T3 Cells
MH  - Phosphorylation
MH  - Protein Isoforms/genetics/metabolism
MH  - Proto-Oncogene Proteins c-met/genetics/*metabolism
MH  - RNA, Messenger/analysis/metabolism
MH  - STAT3 Transcription Factor
MH  - Serum/metabolism
MH  - Thymus Gland
MH  - Trans-Activators/metabolism
EDAT- 2004/09/15 05:00
MHDA- 2005/02/11 09:00
CRDT- 2004/09/15 05:00
PHST- 2004/09/15 05:00 [pubmed]
PHST- 2005/02/11 09:00 [medline]
PHST- 2004/09/15 05:00 [entrez]
AID - 200406301 [pii]
AID - 10.1038/emm.2004.39 [doi]
PST - ppublish
SO  - Exp Mol Med. 2004 Aug 31;36(4):283-91. doi: 10.1038/emm.2004.39.