PMID- 9096674
OWN - NLM
STAT- MEDLINE
DCOM- 19970501
LR  - 20190708
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 71
IP  - 1
DP  - 1997 Mar 28
TI  - Melanoma cell migration on vitronectin: regulation by components of the 
      plasminogen activation system.
PG  - 116-22
AB  - Tumor cell migration and invasion require complex interactions between tumor 
      cells and the surrounding extracellular matrix. These interactions are modified 
      by cell adhesion receptors, as well as by proteolytic enzymes and their 
      receptors. Here, we study the influence of the protease urokinasetype plasminogen 
      activator (uPA) and its receptor (uPAR) on melanoma cell adhesion to, and 
      migration on, the extracellular matrix protein vitronectin (VN). Cell adhesion to 
      VN, but not to type I collagen, is significantly enhanced in the presence of 
      either uPA or its amino-terminal fragment (ATF). Soluble uPAR can inhibit this 
      effect, indicating that uPA/uPAR on melanoma cells can function as a VN receptor. 
      In the absence of bivalent cations, uPA/uPAR can promote cell attachment on VN, 
      but not cell spreading, suggesting that the glycosylphosphatidylinositol 
      (GPI)-anchored uPAR alone is unable to organize the cytoskeleton. Chemotactic 
      melanoma cell migration on a uniform VN matrix is inhibited by uPA and ATF, 
      implying that cell motility decreases when uPA/uPAR acts as a VN receptor. In 
      contrast, plasminogen activator inhibitor I (PAI-I) can stimulate melanoma cell 
      migration on VN, presumably by inhibiting uPA/uPAR-mediated cell adhesion to VN 
      and thereby releasing the inhibition of cell migration induced by uPA. Together, 
      our data implicate components of the plasminogen activation system in the direct 
      regulation of cell adhesion and migration, thereby modulating the behavior of 
      malignant tumor cells.
FAU - Stahl, A
AU  - Stahl A
AD  - Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA.
FAU - Mueller, B M
AU  - Mueller BM
LA  - eng
GR  - CA59692/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (PLAUR protein, human)
RN  - 0 (Plasminogen Activator Inhibitor 1)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, Urokinase Plasminogen Activator)
RN  - 0 (Receptors, Vitronectin)
RN  - 0 (Vitronectin)
RN  - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
SB  - IM
MH  - Cell Movement/drug effects/physiology
MH  - Chemotaxis
MH  - Humans
MH  - Melanoma/*metabolism/pathology
MH  - Plasminogen Activator Inhibitor 1/pharmacology
MH  - Receptors, Cell Surface/*physiology
MH  - Receptors, Urokinase Plasminogen Activator
MH  - Receptors, Vitronectin/drug effects/physiology
MH  - Tumor Cells, Cultured
MH  - Urokinase-Type Plasminogen Activator/*pharmacology
MH  - Vitronectin/drug effects/*metabolism
EDAT- 1997/03/28 00:00
MHDA- 2000/06/20 09:00
CRDT- 1997/03/28 00:00
PHST- 1997/03/28 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/03/28 00:00 [entrez]
AID - 10.1002/(SICI)1097-0215(19970328)71:1<116::AID-IJC19>3.0.CO;2-G [pii]
AID - 10.1002/(sici)1097-0215(19970328)71:1<116::aid-ijc19>3.0.co;2-g [doi]
PST - ppublish
SO  - Int J Cancer. 1997 Mar 28;71(1):116-22. doi: 
      10.1002/(sici)1097-0215(19970328)71:1<116::aid-ijc19>3.0.co;2-g.