Fig. 5

PCa development is triggered by CXC chemokines. In PCa, CXCL1 and receptor (CXCR2) induce PCa cell proliferation via ERK/NF-kB, Akt, and JNK. CXCL2 mobility primarily regulates neutrophils, monocytes, lymphocytes, macrophages, B cells, T cells, CD8⁺ T cells, NK cells, etc., to induce immune cell differentiation and, via NF-kB, PCa formation. CXCL3/CXCR2 is upregulated in PCa and contributes to PCa cell migration, invasion, and growth through the ERK and Akt pathways and the molecule NDRG3. CXCL4/CXCR12 promotes invasive signals and metastatic proliferation via the P13K pathway. CXCL5/CXCR2 via Akt, NF-kB, and ERK1/2 and the molecule MALT1 are critical for PCa cell expression, invasion, and tumor growth. High-NOTCH1 PCa expresses greater CXCL6, which induces metastasis, angiogenesis of PCa, and chemoresistance. CXCL9 attracts effector T cells, which play a key role in the inflammation and promotion of PCa cells. Likewise, CXCL10 recruits effector T cells, which also produce inflammation, and it also causes PCa cell migration and invasion through the NF-kB and TLR4/5 pathways. CXCL11 acts as a tumor suppressor in PCa. CXCL12/CXCR4/CXCR7 induce in PCa cell promote growth and metastasis via MAPK, ERK, Akt pathways while in contrast, wt-p53 pathway inhibits the CXCR4 and CXCL12 in the interactions and inhibited the migration of PCa cells to the bones. CXCL13/CXCR5 are also up-regulated during PCa via the JNK, ERK, and NF-kB pathways, leading to promote PCa cell growth and invasion. The CXCL14 facilitates the EMT in the PCa via the NF-kB pathway. CXCL16/CXCR6 recruits the leukocytes via activation by FAK, P13K, PKC, NF-kB, ERK1/2 pathways, and protein GSK-3b, which promote motility, invasion, and metastasis of PCa. The up (↑) arrow symbol represents upregulation