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Colorectal cancer (CRC) is a typical lifestyle-related disease, and it metastasizesmostly to the liver. It is important to understand the molecular mechanisms ofCRC metastasis in order to design new and effective treatments for CRC patients.Chemokines are known to have antitumor effects as their chemoattractant propertiesstimulate the accumulation of infiltrating immune cells (TILs) in tumors. Chemokine(C-X-C motif) ligand 16 (CXCL16), also known as SR-PSOX, is a unique membrane-boundchemokine that induces the expression of its specific receptor CXCR6. We previouslyreported that the expression of CXCL16 by cancer cells enhances the recruitmentof TILs, thereby improving the prognosis of CRC. It has since been reported thatCXCL16/CXCR6 expression is involved in the metastasis of various types of cancer.However, there is no report of the association between CXCL16 expression and livermetastasis in CRC. In this study, we investigated the role of cancer-derived CXCL16and the possibility of gene therapy using CXCL16. Therefore, we examined the metastasisof colon 38 SL4 cells to the liver in an experimental model. Following injectionof cancer cells into the intraportal vein, CXCL16-expressing CRC cells drasticallyinhibited liver metastasis. We also found that CD8 T cells and natural killer T(NKT) cells, known as CXCR6-expressing cells, increased in CXCL16-expressing metastatictissue. Collectively, the inhibitory effect on metastasis to the liver by CXCL16was observed in NKT cell-depleted mice but not in CD8 T cell-depleted mice. Theseresults demonstrate the inhibitory effect of CXCL16 on liver metastasis via NKTcells in CRC.

Chemokine CXCL16 suppresses liver metastasis of colorectal cancer via augmentation of tumor-infiltrating natural killer T cells in a murine model