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S100A10 Key for Recruitment of Macrophages to Tumor Sites

Reduced murine carcinoma, fibrosarcoma growth in S100A10-deficient versus wild-type mice

MONDAY, Oct. 31 (HealthDay News) -- The plasminogen receptor S100A10 is involved in facilitating movement of macrophages to tumor sites, according to an experimental study published online Oct. 31 in Cancer Research.

Kyle D. Phipps, Ph.D., from Dalhousie University in Halifax, Canada, and colleagues investigated the role of plasminogen receptor S100A10 in recruitment of macrophages to tumor sites. Wild-type and S100A10-null mice were inoculated with Lewis lung carcinoma (LLC) and T241 murine fibrosarcoma cells to examine the kinetics of tumor growth. Peritoneal lavage was used to collect macrophages after tumor cell inoculation, and the proliferative rates of tumor cells were measured in wild-type and S100A10-deficient mice.

The investigators identified reduced growth of murine LLC or T241 fibrosarcomas in S100A10-deficient mice compared with wild-type mice. The decrease in tumor growth correlated with a reduction in macrophage density. Intraperitoneal injection of wild-type, but not S100A1-deficient, macrophages stimulated tumor growth. Injection of wild-type or S100A1-definicent macrophages directly into the tumor stimulated tumor growth. The tumor growth deficit seen in S100A10-deficient mice was phenocopied by selective depletion of macrophages from wild-type mice.

"Although other mechanisms cannot be excluded, we propose that S100A10-dependent plasmin generation plays a critical role in the movement of macrophages to the tumor site. These findings highlight a new therapeutic modality in which tumor progression may be controlled by targeting tumor-associated macrophages," the authors write.

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