ubd介导的糖酵解重编程促进卵巢癌免疫逃避中M2巨噬细胞极化

IF 3.9 3区 生物学 Q3 CELL BIOLOGY
Nana Zhang, Fengming Zhao, Hailong Chen, Juli Wang, Haiyan Li
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引用次数: 0

摘要

卵巢癌(OC)是女性最常见的恶性肿瘤之一,免疫治疗耐药(ITR)是一个主要挑战。糖酵解代谢重编程已被证明在肿瘤免疫微环境和免疫逃避中起着至关重要的作用,但其潜在机制尚不清楚。本研究旨在探讨泛素D (Ubiquitin D, UBD)在OC免疫治疗中的作用,特别是其通过糖酵解代谢调节巨噬细胞极化。利用癌症基因组图谱和临床蛋白质组学肿瘤分析联盟数据库的数据,结合蛋白质组学技术,我们分析了UBD在OC组织中的表达及其与关键糖酵解酶的相关性。通过慢病毒介导的基因操作和体内小鼠模型,我们评估了UBD对巨噬细胞极化、糖酵解代谢和免疫治疗的影响。结果表明,UBD通过糖酵解重编程促进M2巨噬细胞极化,增强OC的免疫逃避和ITR。抑制UBD或靶向糖酵解途径可能为改善OC免疫治疗提供新的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

UBD-mediated glycolytic reprogramming promotes M2 macrophage polarization in ovarian cancer immune evasion

UBD-mediated glycolytic reprogramming promotes M2 macrophage polarization in ovarian cancer immune evasion

Ovarian cancer (OC) is one of the most common malignant tumors in women, with immunotherapy resistance (ITR) being a major challenge. Glycolytic metabolic reprogramming has been shown to play a crucial role in the tumor immune microenvironment and immune evasion, yet the underlying mechanisms remain unclear. This study aims to investigate the role of Ubiquitin D (UBD) in OC immunotherapy, particularly its regulation of macrophage polarization through glycolytic metabolism. Using data from the Cancer Genome Atlas and Clinical Proteomic Tumor Analysis Consortium databases, combined with proteomics techniques, we analyzed the expression of UBD in OC tissues and its correlation with key glycolytic enzymes. Through lentiviral-mediated gene manipulation and in vivo mouse models, we evaluated the effects of UBD on macrophage polarization, glycolytic metabolism, and immunotherapy. The results indicate that UBD promotes M2 macrophage polarization through glycolytic reprogramming, enhancing immune evasion and ITR in OC. Inhibiting UBD or targeting glycolytic pathways may provide new strategies for improving OC immunotherapy.

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来源期刊
CiteScore
6.40
自引率
4.90%
发文量
40
期刊介绍: The Journal of Cell Communication and Signaling provides a forum for fundamental and translational research. In particular, it publishes papers discussing intercellular and intracellular signaling pathways that are particularly important to understand how cells interact with each other and with the surrounding environment, and how cellular behavior contributes to pathological states. JCCS encourages the submission of research manuscripts, timely reviews and short commentaries discussing recent publications, key developments and controversies. Research manuscripts can be published under two different sections : In the Pathology and Translational Research Section (Section Editor Andrew Leask) , manuscripts report original research dealing with celllular aspects of normal and pathological signaling and communication, with a particular interest in translational research. In the Molecular Signaling Section (Section Editor Satoshi Kubota) manuscripts report original signaling research performed at molecular levels with a particular interest in the functions of intracellular and membrane components involved in cell signaling.
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