CX3CL1 and non-small cell lung carcinoma: In this feedback loop, VBMECs provided soluble CX3CL1 in the bone microenvironment, which directly acted on circulating NSCLC cells to stimulate their invasion and increase their adhesion; in turn, circulating NSCLC cells stimulated VBMECs to synthesize and secrete CX3CL1 via several relevant signaling pathways, facilitating the increase in VBMEC permeability and constituting the condition-chain of circulating NSCLC cell transendothelial migration (Figure 8).