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The homophilic binding of junctional adhesion molecule-C mediates tumor cell-endothelial cell interactions

Sentot Santoso1, Valeria V Orlova, Kaimei Song

  • 1Experimental Immunology Branch, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA.

The Journal of Biological Chemistry
|August 25, 2005
PubMed

Insights

Junctional adhesion molecule C (JAM-C) engages in homophilic interactions, mediated by its amino-terminal Ig domain, to facilitate tumor cell adhesion to endothelial cells, potentially aiding metastasis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Junctional adhesion molecule C (JAM-C) is known to interact with leukocyte integrin Mac-1, influencing inflammatory cell recruitment.
  • Understanding JAM-C's interactions is crucial for deciphering cell adhesion processes in both inflammation and cancer.

Purpose of the Study:

  • To characterize the homophilic interaction of JAM-C.
  • To investigate the role of JAM-C homophilic interaction in tumor cell-endothelial cell adhesion.
  • To identify the specific domains and motifs involved in JAM-C homophilic binding.

Main Methods:

  • Utilized recombinant soluble JAM-C and JAM-C-transfected Chinese hamster ovary (CHO) cells in binding assays.
  • Employed site-directed mutagenesis to investigate the role of the Arg64-Ile65-Glu66 motif.
  • Assessed the adhesion of lung carcinoma cells (NCI-H522) to JAM-C expressing cells and endothelial cells.

Main Results:

  • Demonstrated that JAM-C undergoes homophilic binding, mediated by its amino-terminal Ig domain (D1).
  • Identified the Arg64-Ile65-Glu66 motif as essential for JAM-C homophilic interaction, with a specific mutation (E66R) abolishing binding.
  • Showed that JAM-C homophilic interaction mediates the adhesion of lung carcinoma cells to endothelial cells, which can be blocked by soluble JAM-C or its D1 domain.

Conclusions:

  • JAM-C mediates tumor cell-endothelial cell interactions through homophilic binding via its D1 domain and the conserved RVE motif.
  • This homophilic interaction may play a significant role in tumor cell metastasis.
  • Targeting JAM-C homophilic interactions could offer a strategy to inhibit cancer cell dissemination.

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