Oncotarget

Research Papers:

Microenvironment-derived ADAM28 prevents cancer dissemination

Catherine Gérard, Céline Hubeau, Oriane Carnet, Marine Bellefroid, Nor Eddine Sounni, Silvia Blacher, Guillaume Bendavid, Markus Moser, Reinhard Fässler, Agnès Noel, Didier Cataldo _ and Natacha Rocks

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Oncotarget. 2018; 9:37185-37199. https://doi.org/10.18632/oncotarget.26449

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Abstract

Catherine Gérard1, Céline Hubeau1, Oriane Carnet1, Marine Bellefroid1, Nor Eddine Sounni1, Silvia Blacher1, Guillaume Bendavid1,2, Markus Moser3, Reinhard Fässler3, Agnès Noel1, Didier Cataldo1,4,* and Natacha Rocks1,*

1Laboratory of Tumor and Development Biology, GIGA-Cancer and GIGA-I3, GIGA-Research, University of Liege, Liege, Belgium

2ENT Department, University Hospital of Liege, Liege, Belgium

3Max-Planck-Institute of Biochemistry, Department of Molecular Medicine, Martinsried, Germany

4Department of Respiratory Diseases, CHU Liege and University of Liege, Liege, Belgium

*These authors have contributed equally to this work

Correspondence to:

Didier Cataldo, email: didier.cataldo@uliege.be

Keywords: ADAM28; lung; metastasis; CD8+; T lymphocytes

Received: July 27, 2018    Accepted: November 26, 2018    Published: December 14, 2018

ABSTRACT

Previous studies have linked cancer cell-associated ADAM28 expression with tumor progression and metastatic dissemination. However, the role of host-derived ADAM28 in cancer dissemination processes remains unclear.

Genetically engineered-mice fully deficient for ADAM28 unexpectedly display increased lung colonization by pulmonary, melanoma or breast tumor cells. In experimental tumor cell dissemination models, host ADAM28 deficiency is further associated with a decreased lung infiltration by CD8+ T lymphocytes. Notably, naive ADAM28-deficient mice already display a drastic reduction of CD8+ T cells in spleen which is further observed in lungs. Interestingly, ex vivo CD8+ T cell characterization revealed that ADAM28-deficiency does not impact proliferation, migration nor activation of CD8+ T cells. Our data highlight a functional role of ADAM28 in T cell mobilization and point to an unexpected protective role for host ADAM28 against metastasis.


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