Journal
JOURNAL OF IMMUNOLOGY
Volume 191, Issue 6, Pages 3453-3461Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1300171
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Funding
- National Basic Research Program of China [2012CB932500]
- National Science Fund for Distinguished Young Scholars of China [81225021]
- National Natural Science Foundation of China [81101508]
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Mechanisms by which tumor cells metastasize to distant organs still remain enigmatic. Immune cells have been assumed to be the root of metastasis by their fusing with tumor cells. This fusion theory, although interpreting tumor metastasis analogically and intriguingly, is arguable to date. We show in this study an alternative explanation by immune cell-derived microparticles (MPs). Upon stimulation by PMA or tumor cell-derived supernatants, immune cells released membrane-based MPs, which were taken up by H22 tumor cells, leading to tumor cell migration in vitro and metastasis in vivo. The underlying molecular basis was involved in integrin alpha(M)beta(2) (CD11b/CD18), which could be effectively relayed from stimulated innate immune cells to MPs, then to tumor cells. Blocking either CD11b or CD18 led to significant decreases in MP-mediated tumor cell metastasis. This MP-mediated transfer of immune phenotype to tumor cells might also occur in vivo. These findings suggest that tumor cells may usurp innate immune cell phenotypes via MP pathway for their metastasis, providing new insight into tumor metastatic mechanism.
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