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A more recent version of this article appeared on April 1, 2005 Originally published as MBC in Press, 10.1091/mbc.E04-12-1082 on February 2, 2005
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Submitted on December 15, 2004
Revised on January 24, 2005
Accepted on January 25, 2005
v
3 Integrin Cell Surface Expression
*Abramson Family Cancer Research Institute, Department of Cell and Developmental Biology, Department of Pathology and Laboratory Medicine, Department of Bioengineering, Institute for Medicine and Engineering, and ||Howard Hughes Medical Institute, University of Pennsylvania, School of Medicine, Philadelphia, PA 19104
Monitoring Editor: Marianne Bronner-Fraser
Hypoxia-Inducible Factor (HIF) deficient placentas exhibit a number of defects, including changes in cell fate adoption, lack of fetal angiogenesis, hypocellularity, and poor invasion into maternal tissue. HIF is a heterodimeric transcription factor consisting of 
and 
(ARNT) subunits. We used undifferentiated trophoblast stem (TS) cells to characterize HIF-dependent adhesion, migration, and invasion. Arnt-/- and Hif-/- TS cells exhibit reduced adhesion and migration toward vitronectin compared with wildtype cells. Furthermore, this defect is associated with decreased cell surface expression of integrin v3 and significantly decreased expression of this integrin in focal adhesions. Because of the importance of adhesion and migration in tumor progression (in addition to placental development) we examined the affect of culturing B16F0 melanoma cells in 1.5% oxygen (O2). Culturing B16F0 melanoma cells at 1.5% O2 resulted in increased v3 integrin surface expression and increased adhesion to and migration toward vitronectin. Taken together these data suggest that HIF and O2 tension influence placental invasion and tumor migration by increasing cell surface expression of v3 integrin.
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