Zhang Liang, Fu Jiangling, Liu Xiaoliang, Feng Shangzhi, Leng Yuanjing
Department of Urology, First Affiliated Hospital of Jiujiang Medical University, Jiujiang 332000, China.
Department of Clinical Medicine School, First Affiliated Hospital of Jiujiang Medical University, Jiujiang 332000, China.
Cancer Biol Med. 2025 Sep 4;22(8). doi: 10.20892/j.issn.2095-3941.2025.0149.
Prostate cancer is a significant global health issue with inflammation emerging as a critical driver of progression. The prostate tumor microenvironment (TME) is comprised of tumor cells, mesenchymal stem cells, immune cells, cancer-associated fibroblasts, adipocytes, and the extracellular matrix. All of these TME components interact soluble factors, such as growth factors, cytokines, and chemokines. These interactions remodel the TME and drive inflammation and tumor progression. Prolonged inflammation leads to dysregulated activation and infiltration of immune cells in the TME. This process maintains an immunosuppressive environment and facilitates epithelial-to-mesenchymal transition, migration, and invasion. Chronic inflammation causes inflammatory mediators to enter the circulation over time, as evidenced by systemic biomarkers, such as the systemic immune-inflammation index, which links inflammation to disease severity. Interactions between the prostate gland and adipose tissues further exacerbate systemic inflammation. Inflammation in the prostate gland confers resistance to therapy, primes distant metastatic niches, and promotes metastatic spread, resulting in poor clinical outcomes. Therapeutic strategies, such as anti-inflammatory agents and immunotherapies, hold promise in mitigating disease burden. This review explored the immune landscape of systemic inflammation in prostate cancer, discussed the role of the immune landscape in resistance to therapy and metastasis, and offered insights into potential interventions for targeting inflammation to limit prostate cancer burden.
前列腺癌是一个重大的全球健康问题，炎症已成为疾病进展的关键驱动因素。前列腺肿瘤微环境（TME）由肿瘤细胞、间充质干细胞、免疫细胞、癌症相关成纤维细胞、脂肪细胞和细胞外基质组成。所有这些TME成分通过可溶性因子（如生长因子、细胞因子和趋化因子）相互作用。这些相互作用重塑TME并驱动炎症和肿瘤进展。长期炎症导致TME中免疫细胞的激活和浸润失调。这一过程维持了免疫抑制环境，并促进上皮-间充质转化、迁移和侵袭。慢性炎症导致炎症介质随着时间的推移进入循环系统，全身性生物标志物（如全身性免疫炎症指数）证明了这一点，该指数将炎症与疾病严重程度联系起来。前列腺与脂肪组织之间的相互作用进一步加剧了全身性炎症。前列腺炎症会导致对治疗产生抗性、引发远处转移微环境并促进转移扩散，从而导致不良的临床结果。抗炎药物和免疫疗法等治疗策略有望减轻疾病负担。本综述探讨了前列腺癌全身性炎症的免疫格局，讨论了免疫格局在治疗抗性和转移中的作用，并提供了针对炎症以减轻前列腺癌负担的潜在干预措施的见解。
