Microenvironment-derived ADAM28 prevents cancer dissemination
Catherine Gérard1, Céline Hubeau1, Oriane Carnet1
1Laboratory of Tumor and Development Biology, GIGA-Cancer and GIGA-I3, GIGA-Research, University of Liege, Liege, Belgium.
Oncotarget
|January 17, 2019
Summary
Host-derived ADAM28 plays a protective role against cancer metastasis by aiding CD8+ T cell mobilization. ADAM28 deficiency unexpectedly increases tumor cell lung colonization, highlighting its importance in anti-metastasis immunity.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- ADAM28 expression on cancer cells is linked to tumor progression and metastasis.
- The function of host-derived ADAM28 in cancer dissemination remains largely unknown.
Purpose of the Study:
- To investigate the role of host-derived ADAM28 in cancer cell dissemination and anti-tumor immunity.
Main Methods:
- Utilized genetically engineered mice lacking ADAM28.
- Assessed lung colonization by pulmonary, melanoma, and breast tumor cells.
- Analyzed CD8+ T lymphocyte infiltration in spleen and lungs.
- Performed ex vivo characterization of CD8+ T cell proliferation, migration, and activation.
Main Results:
- ADAM28-deficient mice showed increased lung colonization by various tumor cells.
- Host ADAM28 deficiency correlated with reduced CD8+ T lymphocyte infiltration in the lungs.
- ADAM28-deficient mice exhibited significantly fewer CD8+ T cells in spleen and lungs.
- Ex vivo analysis indicated no impact of ADAM28 deficiency on CD8+ T cell proliferation, migration, or activation.
Conclusions:
- Host ADAM28 is crucial for T cell mobilization, particularly CD8+ T cells.
- ADAM28 acts as a protective factor against cancer metastasis.
- This study reveals an unexpected role for host ADAM28 in regulating anti-metastasis immunity.
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