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Related Experiment Videos

Tetraspanin CD82 attenuates cellular morphogenesis through down-regulating integrin alpha6-mediated cell adhesion.

Bo He1, Li Liu, George A Cook

  • 1Vascular Biology Center and Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.

The Journal of Biological Chemistry
|November 24, 2004
PubMed
Summary

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Tetraspanin CD82 inhibits prostate cancer cell morphogenesis by reducing cell surface integrin alpha6. This interaction decreases cell adhesion to laminin, impacting cell motility and invasiveness.

Area of Science:

  • Cell biology
  • Molecular oncology
  • Cancer research

Background:

  • Tetraspanin CD82 is involved in integrin-mediated cell functions.
  • The precise role of CD82 in regulating integrin functionality remains unclear.
  • Prostate cancer cell morphogenesis on Matrigel depends on integrin alpha6.

Purpose of the Study:

  • To investigate the functional cross-talk between CD82 and integrin alpha6.
  • To determine how CD82 affects integrin alpha6-mediated cell adhesion and morphogenesis.
  • To elucidate the mechanism by which CD82 influences cell surface integrin alpha6 levels.

Main Methods:

  • Utilized Du145 prostate cancer cells and Matrigel for morphogenesis assays.
  • Expressed CD82 in Du145 cells to assess its impact on cell behavior.

Related Experiment Videos

  • Analyzed cell adhesion to laminin 1.
  • Quantified cell surface and total levels of integrin alpha6.
  • Investigated physical association between CD82 and integrin alpha6 using co-immunoprecipitation.
  • Assessed the internalization rate of cell surface integrin alpha6.

    • Main Results:

    • CD82 expression abolished integrin alpha6-dependent prostate cancer cell morphogenesis.
    • CD82 significantly inhibited cell adhesion to laminin 1.
    • CD82 expression led to down-regulation of cell surface integrin alpha6 without altering total protein levels.
    • CD82 physically associated with integrin alpha6, forming a complex that reduces cell surface expression.
    • Internalization of cell surface integrin alpha6 was significantly enhanced in CD82-expressing cells.

    Conclusions:

    • CD82 attenuates integrin alpha6 signaling in prostate cancer cell morphogenesis.
    • Reduced cell surface expression of integrin alpha6 due to CD82 is responsible for diminished laminin adhesion and impaired morphogenesis.
    • Accelerated internalization of integrin alpha6 upon CD82 expression correlates with decreased cell surface levels and functional consequences.