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高尔基体蛋白73:免疫和肿瘤微环境中炎症的驱动因素

Golgi protein 73: the driver of inflammation in the immune and tumor microenvironment.

作者信息

Feng Pingping, Hu Xinyang, Zhou Sining, Liu Xianyong, Zeng Linghui, Liu Yiming

机构信息

Hangzhou Lin'an Traditional Chinese Medicine Hospital, Affiliated Hospital, Hangzhou City University, Hangzhou, China.

Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, Hangzhou City University School of Medicine, Hangzhou, China.

出版信息

Front Immunol. 2025 Jan 8;15:1508034. doi: 10.3389/fimmu.2024.1508034. eCollection 2024.

Abstract

Golgi Protein 73 (GP73) is a Golgi-resident protein that is highly expressed in primary tumor tissues. Initially identified as an oncoprotein, GP73 has been shown to promote tumor development, particularly by mediating the transport of proteins related to epithelial-mesenchymal transition (EMT), thus facilitating tumor cell EMT. Though our previous review has summarized the functional roles of GP73 in intracellular signal transduction and its various mechanisms in promoting EMT, recent studies have revealed that GP73 plays a crucial role in regulating the tumor and immune microenvironment. GP73 can modulate intracellular signaling pathways to influence cytokine and chemokine networks, resulting in inflammation caused by viral and bacterial infection or immune diseases, and leading tumor microenvironment deteriorated. Additionally, extracellular GP73 can also regulate signaling pathways of target cells by binding to their cell-surface receptors or entering the acceptor cells, thereby facilitating inflammation or promoting tumor development. In this review, we aim to summarize the findings, providing insights for future investigations on GP73 and its potential as a therapeutic target in ameliorating chronic inflammation in the immune and tumor microenvironment.

摘要

高尔基体蛋白73(GP73)是一种驻留高尔基体的蛋白,在原发性肿瘤组织中高表达。GP73最初被鉴定为一种癌蛋白,已被证明可促进肿瘤发展,特别是通过介导与上皮-间质转化(EMT)相关的蛋白转运,从而促进肿瘤细胞的EMT。尽管我们之前的综述总结了GP73在细胞内信号转导中的功能作用及其促进EMT的各种机制,但最近的研究表明,GP73在调节肿瘤和免疫微环境中起着关键作用。GP73可调节细胞内信号通路,影响细胞因子和趋化因子网络,导致由病毒和细菌感染或免疫疾病引起的炎症,并使肿瘤微环境恶化。此外,细胞外GP73还可通过与靶细胞的细胞表面受体结合或进入受体细胞来调节靶细胞的信号通路,从而促进炎症或肿瘤发展。在本综述中,我们旨在总结这些发现,为未来关于GP73的研究及其作为改善免疫和肿瘤微环境中慢性炎症的治疗靶点的潜力提供见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1943/11750648/15eaa4105e6d/fimmu-15-1508034-g001.jpg

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