前列腺炎是前列腺癌的危险因素之一，核转录因子-κB（nuclear factor κB, NF-κB）在前列腺炎诱发前列腺癌的过程中起重要作用。作为炎症环境特点之一的缺氧与参与免疫应答的Toll样受体，均可激活NF-κB；同时炎症细胞亦可通过NF-κB影响肿瘤的生物学行为；此外，NF-κB与其他前炎症因子间存在交互作用。NF-κB通过多途径调控肿瘤生长，包括促凋亡、抑增殖，介导肿瘤侵袭、转移和血管生成，同时可能诱导前列腺癌向雄激素非依赖性阶段演进。抗炎及针对NF-κB的靶向治疗为前列腺癌的治疗提供新思路，有待进一步深入研究。

Prostatitis is a risk factor of prostate cancer. Nuclear factor-κB (NF-κB) plays an important role in the tumorigenesis of prostate cancer induced by prostatitis. Hypoxia, a marker of inflammation, and Toll like receptors both can activate NF-κB. Inflammatory cells can regulate the biological behavior of tumors through NF-κB. Moreover, NF-κB has a cross-talk with many pro-inflammatory factors. NF-κB regulates tumor growth through various ways, including apoptosis promotion and proliferation suppression, mediation of invasion, metastasis and angiogenesis of tumors; NF-κB also can induce progression of prostate cancer from the androgen-dependent to the androgen-independent stage. Anti-inflammation and NF-κB-targeting therapies cast new lights on prostate cancer treatment, which deserves further study.

国家自然科学基金资助项目（No. 30872591）