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Differential expression of cell-cell adhesion proteins and cyclin D in MEK1-transdifferentiated MDCK cells

I Marschitz1, J Lechner, I Mosser

  • 1Department of Physiology, University of Innsbruck, A-6010 Innsbruck, Austria.

American Journal of Physiology. Cell Physiology
|October 13, 2000
PubMed

Insights

Overexpression of constitutively active MEK1 (caMEK1) in kidney cells disrupts cell adhesion and promotes invasion. This invasive phenotype is linked to reduced cell-cell adhesion proteins and increased cyclin D expression, impacting cell proliferation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Constitutively active MEK1 (caMEK1) overexpression in MDCK-C7 cells disrupts cell morphogenesis and induces an invasive phenotype.
  • The involvement of cell-cell adhesion molecules and cell cycle proteins in caMEK1-induced cellular changes remains unclear.

Purpose of the Study:

  • To investigate the role of cell-cell adhesion molecules and cell cycle proteins in the invasive phenotype induced by caMEK1.
  • To elucidate the molecular mechanisms underlying caMEK1-driven cellular transdifferentiation and invasiveness.

Main Methods:

  • Stable transfection of MDCK-C7 cells with caMEK1 (C7caMEK1) and mock control (C7Mock1).
  • Analysis of E-cadherin, alpha-catenin, and beta-catenin expression using immunoprecipitation and Western blotting.
  • Treatment with proteasome inhibitors (ALLN, lactacystin) to assess beta-catenin stability.
  • Assessment of cyclin D expression and cell proliferation rates in response to MEK inhibitor U-0126.

Main Results:

  • C7caMEK1 cells exhibited loss of E-cadherin and reduced beta- and alpha-catenin expression compared to C7Mock1 cells.
  • Proteasome inhibitors caused beta-catenin accumulation in both cell types.
  • C7caMEK1 cells displayed higher cyclin D expression, which was sensitive to MEK inhibition by U-0126.
  • U-0126 treatment reduced cyclin D expression and cell proliferation in C7caMEK1 cells.

Conclusions:

  • The invasive phenotype of C7caMEK1 cells is associated with diminished cell-cell adhesion protein expression.
  • Reduced beta-catenin expression occurs despite increased cyclin D levels, which are sensitive to MEK/ERK signaling.
  • These findings highlight the interplay between cell adhesion, cell cycle regulation, and invasive potential in caMEK1-expressing cells.

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