Fig. 4

A Model of prostate cancer tumor growth in the bone microenvironment mediated by efferocytosis. Apoptotic cancer cells are engaged and efferocytosis by bone macrophages (MΦs), which activate Stat3 and NF-B (p65), resulting in the release of proinflammatory cytokines such as CCL5, CXCL1, IL-6, and CXCL5. CXCL5 is involved in the chemoattraction of inflammatory myeloid cells such as CD11b⁺Gr-1⁺ and Ly6B⁺ cells, as well as the promotion of M2 (F4/80⁺CD206⁺ cells) polarization, all of which lead to chronic inflammation and immunosuppression that promote tumor growth. B CXCL13 influences the following signaling pathways: interactions with CXCR5. CXCL13 binding to CXCR5 activates the PI3K/Akt, Raf/MEK/ERK, Integrin-3/Src/FAK, and DOCK2/Rac/JNK pathways, all of which are important in cell survival, invasion, and growth