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Inflammation is involved in regulation of cellular events in prostate carcinogenesis through control of the tumour micro‐environment. A variety of bone marrow‐derived cells, including CD 4+ lymphocytes, macrophages and myeloid‐derived suppressor cells, are integral components of the tumour micro‐environment. On activation by inflammatory cytokines, NF ‐κ B complexes are capable of promoting tumour cell survival through anti‐apoptotic signalling in prostate cancer ( PCa ). Positive feedback loops are able to maintain NF ‐κ B activation. NF ‐κ B activation is also associated with the metastatic phenotype and PCa progression to castration‐resistant prostate cancer ( CRPC ). A novel role for inhibitor of NF ‐κ B kinase ( IKK )‐α in NF ‐κ B ‐independent PCa progression to metastasis and CRPC has recently been uncovered, providing a new mechanistic link between inflammation and PCa . Expansion of PCa progenitors by IKK ‐α may be involved in this process. In this review, we offer the latest evidence regarding the role of the NF ‐κ B pathway in PCa and discuss therapeutic attempts to target the NF ‐κ B pathways. We point out the need to further dissect inflammatory pathways in PCa in order to develop appropriate preventive measures and design novel therapeutic strategies.
Nguyen et al. (Mon,) studied this question.
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