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Related Experiment Videos

Hypoxia-inducible factor regulates alphavbeta3 integrin cell surface expression.

Karen D Cowden Dahl1, Sarah E Robertson, Valerie M Weaver

  • 1Abramson Family Cancer Research Institute, School of Medicine, University of Pennsylvania, Philadelphia, 19104, USA.

Molecular Biology of the Cell
|February 4, 2005
PubMed
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Hypoxia-inducible factor (HIF) influences placental invasion and tumor cell migration. Low oxygen increases cell surface expression of integrin alphavbeta3, enhancing adhesion and migration.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Cancer Research

Background:

  • Hypoxia-inducible factor (HIF) plays a critical role in placental development.
  • HIF-deficient placentas show defects in cell fate, angiogenesis, and invasion.
  • HIF is a heterodimer of HIF-alpha and aryl hydrocarbon receptor nuclear translocator (ARNT) subunits.

Purpose of the Study:

  • To investigate the role of HIF in trophoblast stem (TS) cell adhesion, migration, and invasion.
  • To characterize the impact of oxygen tension on integrin expression and cell behavior in melanoma cells.

Main Methods:

  • Utilized undifferentiated trophoblast stem (TS) cells (Arnt(-/-), Hifalpha(-/-), and wild-type).
  • Assessed cell adhesion and migration toward vitronectin.
  • Quantified cell surface and focal adhesion expression of integrin alphavbeta3.

Related Experiment Videos

  • Cultured B16F0 melanoma cells under hypoxic conditions (1.5% O(2)).

    • Main Results:

    • Arnt(-/-) and Hifalpha(-/-) TS cells displayed reduced adhesion and migration to vitronectin.
    • This defect correlated with decreased cell surface and focal adhesion expression of integrin alphavbeta3.
    • Hypoxic culture of B16F0 melanoma cells increased alphavbeta3 integrin surface expression.
    • Hypoxic melanoma cells showed enhanced adhesion to and migration toward vitronectin.

    Conclusions:

    • HIF signaling and oxygen tension regulate placental invasion and tumor cell migration.
    • Increased cell surface expression of integrin alphavbeta3 is a key mechanism mediating these effects.