Fig. 5.

Model of CXCL5/CXCR2 in metastatic bone colonization. Proposed model of the dormancy switch to colonization by CXCL5/CXCR2 axis in cancer cells. Bone marrow cells from healthy bone produce factors that act as sponges for or inhibit CXCL5, making CXCL5 unavailable for binding to its receptor on cancer cells and activating proliferation, thus causing the cancer cells to remain quiescent. In contrast, cancer-primed bone either inhibits or does not produce the factors that inhibit CXCL5. CXCL5 binds and activates its receptor on the cancer cells, ultimately inducing cancer cell proliferation and colonization at the bone metastatic site