Skip to main content

REVIEW article

Front. Immunol.
Sec. Vaccines and Molecular Therapeutics
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1508034

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

Provisionally accepted
Pingping Feng Pingping Feng 1*Xinyang Hu Xinyang Hu 2*Sining Zhou Sining Zhou 2Xianyong Liu Xianyong Liu 1*Linghui Zeng Linghui Zeng 1*Yiming Liu Yiming Liu 1*
  • 1 Hangzhou City University, Hangzhou, China
  • 2 Zhejiang University, Hangzhou, Zhejiang Province, China

The final, formatted version of the article will be published soon.

    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.

    Keywords: Golgi protein 73, Inflammation, cytokine and chemokine networks, Anti-infection immunity, Tumor Microenvironment

    Received: 30 Oct 2024; Accepted: 18 Dec 2024.

    Copyright: © 2024 Feng, Hu, Zhou, Liu, Zeng and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Pingping Feng, Hangzhou City University, Hangzhou, China
    Xinyang Hu, Zhejiang University, Hangzhou, 310058, Zhejiang Province, China
    Xianyong Liu, Hangzhou City University, Hangzhou, China
    Linghui Zeng, Hangzhou City University, Hangzhou, China
    Yiming Liu, Hangzhou City University, Hangzhou, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.