Table 3.

Role of CX3CL1/CX3CR1 axis in cancer.

Gliomas	CX3CL1 negatively regulates glioma cell invasiveness by promoting aggregation of CX3CR1+ tumor cells
Neuroblastoma (NB)	(i) Soluble CX3CL1 stimulates CX3CR1+ NB cells to transmigrate through CX3CR1+/CX3CL1+ human bone-marrow endothelium (ii) Deletion of CX3CL1 gene into NB cell lines induces an antitumor immune response mediated by NK cells and T lymphocytes
Prostate cancer	Soluble CX3CL1 attracts CX3CR1+ prostate cancer cells to the bone marrow and guides their preferential migration towards human osteoblasts
Pancreatic ductal adenocarcinoma (PDAC)	CX3CR1 mediates migration of PDAC cells to CX3CL1 constitutively expressed by neural cells
Epithelial ovarian carcinoma (EOC)	CX3CL1/CX3CR1 axis facilitates cell migration and cell adhesion between EOC cells and peritoneal mesothelial cells
Breast cancer	(i) CX3CR1 contributes to tumor metastasis to skeleton and brain where bone stromal cells and neurons release soluble CX3CL1 (ii) CX3CL1 induces both innate and adaptive immunity and correlates with good prognosis
Colorectal cancer	Soluble CX3CL1, produced by colon cancer cells, attracts cytotoxic effector T lymphocytes and NK cells showing antitumor effects
Hepatocellular carcinoma	CX3CL1/CX3CR1 axis elicits tumor-specific cytotoxic T cell response and correlates with good prognosis
Gastric adenocarcinoma	CX3CL1 promotes both innate and adaptive immunities
B-chronic lymphocytic leukemia (B-CLL)	CX3CL1/CX3CR1 axis, coexpressed on B-CLL cells, is involved in the interaction between leukemic cells and tumor microenvironment
B cell lymphomas	CX3CL1/CX3CR1 axis, coexpressed on lymphoma cells, may be involved in the interaction between lymphoma cells and tumor microenvironment