PMID- 15678502
OWN - NLM
STAT- MEDLINE
DCOM- 20050715
LR  - 20091119
IS  - 0270-4137 (Print)
IS  - 0270-4137 (Linking)
VI  - 64
IP  - 2
DP  - 2005 Jul 1
TI  - Involvement of HGF/SF-Met signaling in prostate adenocarcinoma cells: evidence 
      for alternative mechanisms leading to a metastatic phenotype in Pr-14c.
PG  - 139-48
AB  - BACKGROUND: Hepatocyte growth factor/scatter factor (HGF/SF) facilitates 
      intercellular communication between the epithelial carcinoma and its surrounding 
      stromal tissue during metastatic invasion through interaction with its 
      proto-oncogenic receptor, Met, found on carcinoma cells. This study utilizes the 
      C31/Tag transgenic mouse prostate cancer cell line model in an attempt to 
      characterize the interaction between HGF/SF and Met on the metastatic potential 
      of prostate cancer. METHODS: Exogenous HGF was supplied to the prostate 
      adenocarcinoma cell line (Pr-14) and metastatic cell line (Pr-14c) to evaluate 
      mitogenicity by proliferation assays, morphological characteristics on an 
      extracellular matrix substrate, and motogenic properties using the scatter assay, 
      invasion chambers, and zymogram studies to analyze secretory enzymes produced by 
      the cell lines. RESULTS: RNA and protein analyses show that the cell lines 
      express similar amounts of Met. Pr-14 cells have an increased growth rate 
      following HGF/SF treatment, whereas the metastatic Pr-14c cells show little 
      change. Morphological studies of Pr-14c cells on extracellular matrix demonstrate 
      negligible changes when compared to the tubular formation of Pr-14 cells after 
      HGF/SF stimulation. Motility studies of the metastatic cells following HGF/SF 
      treatment reveal a potentially faulty signaling pathway downstream of Met 
      activation in the metastatic prostate cells. CONCLUSIONS: Our studies suggest 
      that proliferation, invasion, and cell morphological characteristics may be 
      induced independently from the HGF/SF-Met pathway in C31/Tag metastatic prostate 
      cancer cells.
CI  - (c) 2005 Wiley-Liss, Inc.
FAU - MacDougall, Christina A
AU  - MacDougall CA
AD  - Biological Sciences Department, Stanford University, Stanford, CA, USA.
FAU - Vargas, Micaela
AU  - Vargas M
FAU - Soares, Colin R
AU  - Soares CR
FAU - Holzer, Ryan G
AU  - Holzer RG
FAU - Ide, Alexander E
AU  - Ide AE
FAU - Jorcyk, Cheryl L
AU  - Jorcyk CL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Prostate
JT  - The Prostate
JID - 8101368
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - Adenocarcinoma/*genetics/physiopathology
MH  - Animals
MH  - Cell Line, Tumor
MH  - Disease Models, Animal
MH  - Hepatocyte Growth Factor/*genetics/physiology
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Neoplasm Invasiveness
MH  - Neoplasm Metastasis
MH  - Phenotype
MH  - Prostatic Neoplasms/*genetics/physiopathology
MH  - Proto-Oncogene Proteins c-met/*genetics/physiology
MH  - Signal Transduction/genetics
EDAT- 2005/01/29 09:00
MHDA- 2005/07/16 09:00
CRDT- 2005/01/29 09:00
PHST- 2005/01/29 09:00 [pubmed]
PHST- 2005/07/16 09:00 [medline]
PHST- 2005/01/29 09:00 [entrez]
AID - 10.1002/pros.20226 [doi]
PST - ppublish
SO  - Prostate. 2005 Jul 1;64(2):139-48. doi: 10.1002/pros.20226.