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Locally applied TCP inhibits tumor growth via possible activation of macrophages
Author(s) -
Naito Yukiko,
Nagata Tomoko,
Tachibana Shigehiro,
Okimoto Mari,
Ohara Naoki,
Hakamatsuka Yasuharu,
Cheng Jinyan
Publication year - 2010
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.32367
Subject(s) - materials science , cancer research , composite material , biology
The aim of this study was to investigate whether beta‐tricalcium phosphate (TCP) inhibits cancer growth, because TCP, a widely used bone replacement material, is known to attract immune cells. Human colon cancer (WiDr) cells were subcutaneously injected on the backs of nude mice, and tumor growth was observed. Seven days after the injection, five animals were implanted with TCP at the tumor sites, five animals were treated by a direct application of 0.12 mg cisplatin at the sites, and four animals were not treated, as a control. Tumor size on the 43rd day of implantation was 1173 mm 3 in the TCP group and was smaller than that in the control, 1621 mm 3 . This inhibition was comparable to that with cisplatin. Furthermore, tumor‐growing rate in the TCP group was significantly lower than that in the control group. Histopathological examination of the tumors showed migration of macrophages only in the TCP group, with TCP particles remaining at the implantation loci. There were no between‐group differences in neutrophil infiltration and angiogenesis. In another series of in vitro experiments, a concentration‐dependent increase in luminol chemiluminescence was observed in isolated human peripheral neutrophils incubated with TCP, and the chemiluminescence due to phagocytosis of opsonized zymosan in the presence of TCP occurred with a lower level of TCP than when the chemiluminescence was due to TCP alone. These results suggest that subcutaneously implanted TCP inhibits tumor growth of implanted WiDr cells, and that the activation by TCP of macrophages plays a role in that inhibition. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2010