Fig. 3

Proinflammatory cytokines (interleukins) play a role in PCa, as depicted in the illustration. IL-1 and the family’s members, including IL-α and IL-β, engage with several pathways, including NF-kB, STAT3, JNK, and MAPK, as well as proteins/molecules such as STAMP2, LCN2, ELF3, and PSGR, to promote PCa cell proliferation, survival, and bone metastasis. The PI3K/Akt/NF-kB pathways are responsible for IL-4-induced AR activation in PCa. Whereas the STAT6 pathway contributed to the development of PCa. IL-6 links with various signaling pathways, including NF-kB, STAT3, and Akt, as well as proteins and molecules such as KMT12D, Gankyrin/NONO/AR, HMGB1/GHRT1/Twsit1, and ROS, to facilitate the migration and proliferation of PCa cells. IL-7 stimulates MMP3 and MMP7 synthesis and activates the Akt/NF-kB pathway, which promotes PCa cell movement and invasion, while the STAT5, JAK, and ERK pathways promote EMT and metastasis. IL-8 stimulates PCa proliferation, migration, invasion, and defense against apoptosis via the NF-kB/STAT3/Akt pathway. IL-8/CXCR2 pathway activation and AR signaling disruption increase PCa NED and malignancy following Wnt4/TCF7L1 induction. IL-9 stimulates mast cell activation to enhance prostate carcinogenesis. AR signaling increases IL-10 and myeloid cell-1 (TREM-1) signaling on macrophages and improves PCa cell motility and invasion. Prostate microenvironment stromal cells’ paracrine IL-11 production via IL-11R–STAT3 signaling promotes PCa cell growth and invasiveness. IL-6 and TNF-α work as risk factors in PCa development. IL-17F triggered the PI3K/Akt signaling pathway to increase PCa cell malignancy, and the IL-17/CTSK axis controls PCa growth and proliferation. PCa membrane-bound TGF-α stimulates EGFR on osteoblasts during bone metastasis through cell-to-cell adhesion. Autocrine ERK signaling and PGE2 production by active EGFR increase bone development. The essential oncogene protein GOLM1 induces EMT in PCa by activating the TGF-β1/Smad2 signaling pathway. The up arrow (↑) symbol represents upregulation