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Updated: Jul 9, 2026

In vitro Cell Migration and Invasion Assays
09:55

In vitro Cell Migration and Invasion Assays

Published on: June 1, 2014

Aminopeptidase N (APN)/CD13-dependent CXCR4 downregulation is associated with diminished cell migration,

Jens Wulfaenger1, Susanna Niedling, Dagmar Riemann

  • 1Martin-Luther-University, Institute of Medical Immunology, Halle-Wittenberg, Germany.

Molecular Membrane Biology
|December 22, 2007
PubMed

Insights

Enzymatically active Aminopeptidase N (APN/CD13) significantly reduces kidney cell proliferation and migration. This occurs by downregulating the CXCR4 receptor, antagonizing SDF-1alpha/CXCL12 signaling.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Aminopeptidase N (APN/CD13) is a ubiquitous membrane-bound protease with diverse functions, including peptide hydrolysis, cell motility modulation, and viral receptor activity.
  • Understanding the distinct roles of enzymatically active versus inactive APN/CD13 is crucial for elucidating its biological significance.

Purpose of the Study:

  • To investigate the functional differences between enzymatically active and inactive Aminopeptidase N (APN/CD13) in human embryonic kidney cells.
  • To determine the impact of APN/CD13 enzymatic activity on cell proliferation, migration, and anchorage-independent growth.

Main Methods:

  • Site-directed mutagenesis was used to create enzymatically inactive APN/CD13 variants.
  • These variants and wild-type APN were stably transfected into human embryonic kidney cells.
  • Cell proliferation, migration, anchorage-independent growth, CXCR4 expression, and SDF-1alpha/CXCL12-mediated migration were analyzed.

Main Results:

  • Wild-type APN transfectants displayed strong enzymatic activity, while all variants were inactive.
  • Active APN expression significantly decreased cell proliferation, migration, and anchorage-independent growth compared to inactive variants and controls.
  • This effect was linked to downregulated mRNA and protein expression of the chemokine receptor CXCR4 and inhibited SDF-1alpha/CXCL12-mediated migration.

Conclusions:

  • High Aminopeptidase N enzyme activity antagonizes cellular properties regulated by the CXCR4/SDF-1alpha system in embryonic kidney cells.
  • The enzymatic function of APN/CD13 plays a critical role in modulating cell behavior beyond its protease activity.

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