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Repression of Wnt-5a impairs DDR1 phosphorylation and modifies adhesion and migration of mammary cells

M Jönsson1, T Andersson

  • 1Division of Experimental Pathology, Lund University, Malmö University Hospital, SE-205 02 Malmö, Sweden. marzieh.jonsson@pat.mas.lu.se

Journal of Cell Science
|August 9, 2001
PubMed

Insights

Wnt-5a protein regulates mammary cell adhesion and migration via collagen interactions. It is essential for activating discoidin domain receptor 1 (DDR1) phosphorylation, impacting cell behavior.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Wnt-5a is a secreted protein involved in embryogenesis and tissue development.
  • Wnt-5a mRNA is expressed in human and mouse mammary cell lines.
  • The precise mechanisms of Wnt-5a's function are not fully understood.

Purpose of the Study:

  • To investigate the biological role of Wnt-5a in the human mammary epithelial cell line HB2.
  • To explore Wnt-5a's influence on cell adhesion, migration, and collagen receptor signaling.

Main Methods:

  • Utilized an antisense approach to repress endogenous Wnt-5a expression.
  • Generated cell populations with constitutive Wnt-5a overexpression.
  • Assessed cell-to-collagen binding, migration through collagen matrices, and discoidin domain receptor 1 (DDR1) phosphorylation.

Main Results:

  • Wnt-5a overexpression enhanced cell-to-collagen binding and reduced hepatocyte growth factor-stimulated migration.
  • Wnt-5a repression led to cell scattering, impaired cell-collagen interaction, and increased motility.
  • Wnt-5a deficiency resulted in failed DDR1 phosphorylation, while Wnt-5a expression enabled it.

Conclusions:

  • Wnt-5a protein regulates mammary epithelial cell adhesion and migration through collagen matrices.
  • Wnt-5a is a necessary co-factor for collagen-induced activation of DDR1 receptors.
  • Wnt/beta-catenin signaling pathway activation did not affect Wnt-5a's role in DDR1 phosphorylation.

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