在这项研究中，我们探索了指导去势抵抗性前列腺癌 (CRPC) 进展的分子动力学，该过程受幽门螺杆菌 (H. pylori) 介导的巨噬细胞 M2 极化通过 IL-17RA/CTSK/EMT 轴的影响。一项 830 名患者参与的临床试验将受试者分为激素敏感型前列腺癌 (HSPC) 和 CRPC 组。通过 ELISA 评估，幽门螺杆菌感染在 CRPC 患者中的发病率较高，影响总生存期 (OS) 和无进展生存期。深入的体外和体内实验，包括16S rDNA测序、免疫组织化学测试和转录组分析，揭示了幽门螺杆菌通过上调IL-17RA和CTSK来促进CRPC生长和转移，从而增强EMT。值得注意的是，M2 巨噬细胞成为影响 CRPC 进展的关键免疫细胞。这项研究揭示了一种新的途径，其中幽门螺杆菌富集通过诱导巨噬细胞 M2 极化、IL-17RA/CTSK 表达和 EMT 激活来加剧 CRPC，揭示了以前未被认识的导致 CRPC 生长和转移的机制。© 2024。作者获得施普林格自然有限公司的独家许可。

In this investigation, we explored the molecular dynamics guiding the progression of castration-resistant prostate cancer (CRPC) influenced by Helicobacter pylori (H. pylori)-mediated M2 polarization of macrophages through the IL-17RA/CTSK/EMT axis. An 830-patient clinical trial categorized subjects into hormone-sensitive prostate cancer (HSPC) and CRPC groups. H. pylori infection, evaluated by ELISA, exhibited a higher incidence in CRPC patients, impacting overall survival (OS) and progression-free survival. In-depth in vitro and in vivo experiments, including 16S rDNA sequencing, immunohistochemical tests, and transcriptome analysis, unveiled that H. pylori promotes CRPC growth and metastasis by upregulating IL-17RA and CTSK, leading to enhanced EMT. Notably, M2 macrophages emerged as pivotal immune cells influencing CRPC progression. This study uncovers a novel pathway wherein H. pylori enrichment exacerbates CRPC by inducing macrophage M2 polarization, IL-17RA/CTSK expression, and EMT activation, shedding light on a previously unrecognized mechanism contributing to the growth and metastasis of CRPC.© 2024. The Author(s), under exclusive licence to Springer Nature Limited.