Cargando…

Microenvironment-derived ADAM28 prevents cancer dissemination

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Gérard, Catherine, Hubeau, Céline, Carnet, Oriane, Bellefroid, Marine, Sounni, Nor Eddine, Blacher, Silvia, Bendavid, Guillaume, Moser, Markus, Fässler, Reinhard, Noel, Agnès, Cataldo, Didier, Rocks, Natacha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6324684/
https://www.ncbi.nlm.nih.gov/pubmed/30647853
http://dx.doi.org/10.18632/oncotarget.26449
Descripción
Sumario: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.