Research Center for Experimental Medicine, State Key Laboratory of Medical Genomics, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Shanghai Model Organisms Center, Shanghai, 201321, China.
Cancer Immunol Immunother. 2024 Jun 4;73(8):143. doi: 10.1007/s00262-024-03730-5.
This study investigates the role of USP47, a deubiquitinating enzyme, in the tumor microenvironment and its impact on antitumor immune responses. Analysis of TCGA database revealed distinct expression patterns of USP47 in various tumor tissues and normal tissues. Prostate adenocarcinoma showed significant downregulation of USP47 compared to normal tissue. Correlation analysis demonstrated a positive association between USP47 expression levels and infiltrating CD8 T cells, neutrophils, and macrophages, while showing a negative correlation with NKT cells. Furthermore, using Usp47 knockout mice, we observed a slower tumor growth rate and reduced tumor burden. The absence of USP47 led to increased infiltration of immune cells, including neutrophils, macrophages, NK cells, NKT cells, and T cells. Additionally, USP47 deficiency resulted in enhanced activation of cytotoxic T lymphocytes (CTLs) and altered T cell subsets within the tumor microenvironment. These findings suggest that USP47 plays a critical role in modulating the tumor microenvironment and promoting antitumor immune responses, highlighting its potential as a therapeutic target in prostate cancer.
本研究探讨了去泛素化酶 USP47 在肿瘤微环境中的作用及其对抗肿瘤免疫反应的影响。TCGA 数据库的分析显示，USP47 在各种肿瘤组织和正常组织中的表达模式存在明显差异。与正常组织相比，前列腺腺癌中 USP47 的表达明显下调。相关性分析表明，USP47 表达水平与浸润性 CD8 T 细胞、中性粒细胞和巨噬细胞呈正相关，与 NKT 细胞呈负相关。此外，使用 Usp47 敲除小鼠观察到肿瘤生长速度较慢且肿瘤负担减轻。缺乏 USP47 导致免疫细胞浸润增加，包括中性粒细胞、巨噬细胞、NK 细胞、NKT 细胞和 T 细胞。此外，USP47 缺乏导致细胞毒性 T 淋巴细胞 (CTL) 的激活增强，并改变了肿瘤微环境中的 T 细胞亚群。这些发现表明，USP47 在调节肿瘤微环境和促进抗肿瘤免疫反应中发挥着关键作用，强调了其作为前列腺癌治疗靶点的潜力。
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