铜代谢在肿瘤免疫中的作用及其在肿瘤治疗中的应用
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作者单位:

1.河南中医药大学第一附属医院检验科;2.郑州大学第一附属医院检验科

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河南省自然科学基金资助项目(编号:162300410299),国家自然科学基金(编号:82100240)


The role of copper metabolism in tumor development and tumor immunity
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Affiliation:

1.Department of Clinical Laboratory, the First Affiliated Hospital of Henan University of Chinese Medicine;2.Department of Clinical Laboratory, First Affiliated Hospital of Zhengzhou University

Fund Project:

Supported by Natural Science Foundation of Henan Province (No. 162300410299), National Natural Science Foundation of China (No. 82100240)

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    摘要:

    【摘要】 铜(Cu)是一种人体必需的微量元素,以氧化和还原形式参与多种代谢和信号传导过程。它与肿瘤发展的多个方面紧密相关,铜稳态的变化对肿瘤细胞的生长、转移、肿瘤微环境的调节、氧化应激反应、细胞信号传递,以及肿瘤细胞逃避免疫监视等过程都有显著影响。在肿瘤细胞中,铜代谢主要通过调节程序性死亡配体1(programmed Death-Ligand 1,PD-L1)的表达来促进肿瘤的免疫逃逸。鉴于铜在肿瘤免疫中的重要作用,调节铜代谢已成为一种有前景的治疗策略。本文综述了铜在人体内的调控机制,探讨了铜代谢紊乱如何影响肿瘤的发生、发展,以及免疫和肿瘤微环境。同时,还探讨了将铜作为肿瘤免疫治疗靶点的研究价值。

    Abstract:

    [Abstract] Copper is an essential trace element that participates in a variety of metabolic and signaling processes in both oxidized and reduced forms.It is closely related to several aspects of tumor development, and changes in copper homeostasis have a significant impact on processes such as tumor cell growth, metastasis, regulation of the tumor microenvironment, oxidative stress, cell signaling, and the escape of tumor cells from immune surveillance.In tumor cells, copper metabolism promotes immune escape from tumors mainly by regulating the expression of programmed death ligand 1 (programmed Death-Ligand 1,PD-L1).Given the important role of copper in tumor immunity, modulating copper metabolism has emerged as a promising therapeutic strategy.This paper reviews the mechanisms of copper regulation in the human body and explores how disturbances in copper metabolism affect tumorigenesis and progression, as well as the immune and tumor microenvironment.The research value of using copper as a target for tumor immunotherapy is also discussed, providing a theoretical basis for future research directions and clinical applications.

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  • 收稿日期:2024-09-30
  • 最后修改日期:2025-02-14
  • 录用日期:2025-05-26
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