Thus, we revealed a negative immune regulatory function for non-platelet-derived CXCL4 through CXCR3 that cancer cells could hijack to evade the host immune system, suggesting that the CXCL4/CXCR3 axis may serve as a novel target for colorectal cancer immunotherapy.
Further, this review, tied with important findings from our laboratory, demonstrates that polyphenols induce CXCR3 expression on regulatory T cells and increases CXCR3 ligands in the tumor microenvironment, which act together to suppress colorectal cancer through a differential mechanism discussed herewith.
In addition, higher CXCR3 expression was associated with distant metastasis (yes vs no: pooled relative ratio [RR] =1.828, 95% CI: 1.140-2.931, <i>P</i>=0.012) in solid tumors and indicated advanced tumor stage (III/IV vs I/II, RR =2.656, 95% CI: 1.809-3.900, <i>P</i><0.001) and lymph node metastasis (yes vs no: RR =2.28, 95% CI: 1.61-3.25, <i>P</i><0.001) in colorectal cancer.
We discovered several pathways that were significantly associated with survival of glioblastoma patients and two whose scores are predictive of survival in colorectal cancer: CXCR3-mediated signaling and oxidative phosphorylation.