RAI16 maintains intestinal homeostasis and inhibits NLRP3‐dependent IL‐18/CXCL16‐induced colitis and the progression of colitis‐associated colorectal cancer

By migration assay, we demonstrated that RAI16–/– TAMs or recombinant mouse CXCL16 (rmCXCL16, 10 ng/ml) treatment could recruit much more MDSCs (Figure 4H). [...]TAM- s or rmCXCL16 treatment could enhance the proliferation and migration of HCT116 cells (Figure 4I and J). According to public data sets, RAI16 mRNA expression was reduced in IBD patients and human CRC tissues and associated with tumour metastasis and overall survival (Figure S2), suggesting a causal link between RAI16 reduction and IBD and CRC pathogenesis. The pro-atherogenic cytokine interleukin-18 induces CXCL16 expression in rat aortic smooth muscle cells via MyD88, interleukin-1 receptor-associated kinase, tumor necrosis factor receptor-associated factor 6, c-Src, phosphatidylinositol 3-kinase, Akt, c-Jun N-terminal kinase, and activator protein-1 signaling.