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How platelet aggregation affects B16BL6 melanoma cell trafficking
Author(s) -
Koike Chieko,
Watanabe Manabu,
Isoai Atsushi,
Kumagai Hiromichi,
Tsukada Hideo,
Irimura Tatsuro,
Okada Shoji,
Oku Naoto
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00441-4
Subject(s) - platelet , melanoma , metastasis , chemistry , in vivo , cancer research , cell , microbiology and biotechnology , pathology , medicine , immunology , cancer , biology , biochemistry
In blood‐borne metastasis, intravasated metastatic tumor cells are thought to localize at the target site via a series of processes involving platelet aggregation, adhesion to endothelium, and invasion through the basal membrane. In the present study, we examined how platelet aggregation contributes to the trafficking of metastatic tumor cells in vivo by use of an inhibitor of platelet aggregation. Highly invasive B16BL6 melanoma cells were labeled with [2‐ 18 F]2‐fluoro‐2‐deoxy‐ d ‐glucose and injected into mice to determine cell trafficking non‐invasively by positron emission tomography. Both platelet aggregation inhibitor cyclo(RSarDPhg), which could not inhibit metastasis, and metastatic inhibitor cyclo(GRGDSPA) suppressed the accumulation of B16BL6 cells in the lung by about 12%, suggesting that platelet aggregation partly affects cell trafficking but not to a great extent, and that platelet aggregation is not the essential step for B16BL6 cell arrest in targets.