Abstract
Abstract CXCL10 is a chemokine, which takes a significant role in migration and proliferation of T cells. It binds to the receptor CXCR3 and is induced in a wide variety of cell types. We have reported in our previous study that RANKL promotes the expression of CXCL10 in osteoclast precursors and, in turn, CXCL10 mediates RANKL expression in T cells in the synovium. Auto-amplification loop of CXCL10 has been acknowledged to be involved in bone destruction of rheumatoid arthritis. However, the role of CXCL10 in bone metastatic destruction remains largely unknown. We are currently conducting further research on the potential role of CXCL10 in bone resorption and bone metastasis. In this study, the synergistic production of CXCL10 was found in co-culture of bone marrow cells and cancer cells in the presence of RANKL. In addition, the serum level of CXCL10 was increased in bone metastatic mice. The CXCL10 deficient mice showed less metastatic lesions in long bone compared to wild mice. Furthermore, treatment with neutralizing antibody to CXCL10 and antagonist for CXCL10 and CXCR3 interaction significantly inhibited the infiltration of tumor cells into long bone and increased the mice survival rate. Therefore, CXCL10 might be an important therapeutic target in the prevention of bone destruction in bone metastasis.
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