PMID- 16951184
OWN - NLM
STAT- MEDLINE
DCOM- 20071126
LR  - 20120604
IS  - 1538-7445 (Electronic)
IS  - 0008-5472 (Linking)
VI  - 66
IP  - 17
DP  - 2006 Sep 1
TI  - Mimp, a mitochondrial carrier homologue, inhibits Met-HGF/SF-induced scattering 
      and tumorigenicity by altering Met-HGF/SF signaling pathways.
PG  - 8687-97
AB  - We have recently shown that Mimp, a mitochondrial carrier protein homologue, is 
      induced by Met-hepatocyte growth factor/scatter factor (HGF/SF) signaling and 
      decreases the mitochondrial membrane potential in DA3 mammary adenocarcinoma 
      cells. We show here that induction of Mimp leads to growth arrest in response to 
      HGF/SF by arresting cells at the S phase of the cell cycle. Induction of Mimp or 
      its transient expression does not lead to apoptosis. Mimp also attenuates 
      HGF/SF-induced cellular scattering in vitro and tumor growth in vivo. The 
      exogenous induction of Mimp at levels similar to its endogenous induction by 
      HGF/SF increases the level of the Met protein and its phosphorylation by HGF/SF 
      but reduces the levels of Shc and prevents the HGF/SF-induced tyrosine 
      phosphorylation of Grb2 and Shc. In contrast, the level of phosphatidylinositol 
      3-kinase (PI3K) increases following Mimp induction and the level of 
      phosphorylated PI3K in response to HGF/SF is unaffected by the exogenous 
      induction of Mimp. Moreover, exogenous Mimp prevents the HGF/SF-induced 
      transcription of the serum response element-luciferase reporter gene. Our results 
      show that Mimp expression reduces Met-HGF/SF-induced proliferation and scattering 
      by attenuating and altering the downstream signaling of Met. These data show a 
      new link between a tyrosine kinase growth factor receptor and a mitochondrial 
      carrier homologue that regulates cellular growth, motility, and tumorigenicity.
FAU - Leibowitz-Amit, Raya
AU  - Leibowitz-Amit R
AD  - Department of Human Microbiology, Sackler Faculty of Medicine, Tel-Aviv 
      University, Tel Aviv, Israel.
FAU - Tsarfaty, Galia
AU  - Tsarfaty G
FAU - Abargil, Yamit
AU  - Abargil Y
FAU - Yerushalmi, Gil M
AU  - Yerushalmi GM
FAU - Horev, Judith
AU  - Horev J
FAU - Tsarfaty, Ilan
AU  - Tsarfaty I
LA  - eng
GR  - P50CA93990/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (HGF protein, human)
RN  - 0 (Membrane Transport Proteins)
RN  - 0 (Mitochondrial Membrane Transport Proteins)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Mtch2 protein, mouse)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Receptors, Growth Factor)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 2.7.10.1 (MET protein, human)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - Breast Neoplasms
MH  - Cell Line
MH  - Cell Line, Tumor
MH  - Female
MH  - Hepatocyte Growth Factor/*physiology
MH  - Humans
MH  - Kidney
MH  - Membrane Transport Proteins/*physiology
MH  - Mitochondrial Membrane Transport Proteins
MH  - Mitochondrial Proteins/*physiology
MH  - Proto-Oncogene Proteins/*physiology
MH  - Proto-Oncogene Proteins c-met
MH  - Receptors, Growth Factor/*physiology
MH  - Signal Transduction
MH  - Transfection
EDAT- 2006/09/05 09:00
MHDA- 2007/12/06 09:00
CRDT- 2006/09/05 09:00
PHST- 2006/09/05 09:00 [pubmed]
PHST- 2007/12/06 09:00 [medline]
PHST- 2006/09/05 09:00 [entrez]
AID - 66/17/8687 [pii]
AID - 10.1158/0008-5472.CAN-05-2294 [doi]
PST - ppublish
SO  - Cancer Res. 2006 Sep 1;66(17):8687-97. doi: 10.1158/0008-5472.CAN-05-2294.