PMID- 16024725
OWN - NLM
STAT- MEDLINE
DCOM- 20051229
LR  - 20220330
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 102
IP  - 30
DP  - 2005 Jul 26
TI  - Proliferation and invasion: plasticity in tumor cells.
PG  - 10528-33
AB  - Invasive and proliferative phenotypes are fundamental components of malignant 
      disease, yet basic questions persist about whether tumor cells can express both 
      phenotypes simultaneously and, if so, what are their properties. Suitable in 
      vitro models that allow characterization of cells that are purely invasive are 
      limited because proliferation is required for cell maintenance. Here, we describe 
      glioblastoma cells that are highly invasive in response to hepatocyte growth 
      factor/scatter factor (HGF/SF). From this cell population, we selected subclones 
      that were highly proliferative or displayed both invasive and proliferative 
      phenotypes. The biological activities of invasion, migration, urokinase-type 
      plasminogen activation, and branching morphogenesis exclusively partitioned with 
      the highly invasive cells, whereas the highly proliferative subcloned cells 
      uniquely displayed anchorage independent growth in soft agar and were highly 
      tumorigenic as xenografts in immune-compromised mice. In response to HGF/SF, the 
      highly invasive cells signal through the MAPK pathway, whereas the selection of 
      the highly proliferative cells coselected for signaling through Myc. Moreover, in 
      subcloned cells displaying both invasive and proliferative phenotypes, both 
      signaling pathways are activated by HGF/SF. These results show how the 
      mitogen-activated protein kinase and Myc pathways can cooperate to confer both 
      invasive and proliferative phenotypes on tumor cells and provide a system for 
      studying how transitions between invasion and proliferation can contribute to 
      malignant progression.
FAU - Gao, Chong-Feng
AU  - Gao CF
AD  - Laboratory of Molecular Oncology, Van Andel Research Institute, 333 Bostwick 
      Avenue Northeast, Grand Rapids, MI 49503, USA.
FAU - Xie, Qian
AU  - Xie Q
FAU - Su, Yan-Li
AU  - Su YL
FAU - Koeman, Julie
AU  - Koeman J
FAU - Khoo, Sok Kean
AU  - Khoo SK
FAU - Gustafson, Margaret
AU  - Gustafson M
FAU - Knudsen, Beatrice S
AU  - Knudsen BS
FAU - Hay, Rick
AU  - Hay R
FAU - Shinomiya, Nariyoshi
AU  - Shinomiya N
FAU - Vande Woude, George F
AU  - Vande Woude GF
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050715
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 67256-21-7 (Hepatocyte Growth Factor)
SB  - IM
MH  - Animals
MH  - Carcinogenicity Tests
MH  - Cell Line, Tumor
MH  - *Cell Proliferation
MH  - Female
MH  - Glioblastoma/*pathology/physiopathology
MH  - Hepatocyte Growth Factor
MH  - Humans
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Neoplasm Invasiveness
MH  - *Phenotype
MH  - Signal Transduction/*physiology
PMC - PMC1180792
EDAT- 2005/07/19 09:00
MHDA- 2005/12/31 09:00
PMCR- 2006/01/26
CRDT- 2005/07/19 09:00
PHST- 2005/07/19 09:00 [pubmed]
PHST- 2005/12/31 09:00 [medline]
PHST- 2005/07/19 09:00 [entrez]
PHST- 2006/01/26 00:00 [pmc-release]
AID - 0504367102 [pii]
AID - 010210528 [pii]
AID - 10.1073/pnas.0504367102 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10528-33. doi: 
      10.1073/pnas.0504367102. Epub 2005 Jul 15.