Journal
LEUKEMIA
Volume 32, Issue 3, Pages 736-743Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2017.287
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Funding
- University of Bari 'Aldo Moro'-Internal Medicine Residency Program
- DFG [FOR 1586 SKELMET, KFO 216]
- Interdisziplinares Zentrum fur Klinische Forschung of the University of Wurzburg [IZKF-B233]
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Cell adhesion in the multiple myeloma (MM) microenvironment has been recognized as a major mechanism of MM cell survival and the development of drug resistance. Here we addressed the hypothesis that the protein junctional adhesion molecule-A (JAM-A) may represent a novel target and a clinical biomarker in MM. We evaluated JAM-A expression in MM cell lines and in 147 MM patient bone marrow aspirates and biopsies at different disease stages. Elevated JAM-A levels in patient-derived plasma cells were correlated with poor prognosis. Moreover, circulating soluble JAM-A (sJAM-A) levels were significantly increased in MM patients as compared with controls. Notably, in vitro JAM-A inhibition impaired MM migration, colony formation, chemotaxis, proliferation and viability. In vivo treatment with an anti-JAM-A monoclonal antibody (alpha JAM-A moAb) impaired tumor progression in a murine xenograft MM model. These results demonstrate that therapeutic targeting of JAM-A has the potential to prevent MM progression, and lead us to propose JAM-A as a biomarker in MM, and sJAM-A as a serum-based marker for clinical stratification.
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