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ORIGINAL RESEARCH article

Front. Cell Dev. Biol.

Sec. Cancer Cell Biology

Volume 13 - 2025 | doi: 10.3389/fcell.2025.1554705

This article is part of the Research Topic Hepatobiliary tumors: Molecular Targets and Therapeutics View all 3 articles

Dendritic cell-derived MYD88 potentiates as a biomarker for immune regulation in hepatocellular carcinoma and may predict a better immunological result

Provisionally accepted
  • 1 Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hebei Province, China
  • 2 Department of Pediatrics, Renmin Hospital of Wuhan University, Wuhan, Hebei Province, China
  • 3 Department of Rehabilitation Medicine, Renmin Hospital of Wuhan University, Wuhan, China
  • 4 Department of Breast, Renmin Hospital of Wuhan University, Wuhan, China

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

    MYD88 (myeloid differentiation primary response 88) is a key adaptor protein mediate immune responses, primarily through Toll-like receptors (TLRs) and interleukin-1 receptor (IL-1R) signaling. The TLR/MYD88 pathway plays a critical role in dendritic cells (DC) maturation and function, contributing to the body's innate immunity. Recent studies have further highlighted MYD88's pivotal role in intrinsic immunity and its regulatory influence on the tumor microenvironment (TME) in hepatocellular carcinoma (HCC). The expression of MYD88 in DCs and its regulatory role in the TME have gained increasing attention. Our pan-cancer data analysis further highlights the significant impact of MYD88 on clinical outcomes in HCC.Analysis of TCGA and GEO databases confirms that MYD88 serves as a key signaling molecule in DCs, reinforcing its critical role in immune regulation. Our in vitro experiments demonstrates that MyD88 modulates T cell function through DCs.In vivo, H22 tumor cells exhibited accelerated growth in MyD88 knockout mice and a reduced response to anti-PD-1 treatment, whereas wild-type mice showed the opposite trend. These findings underscore the critical role of MYD88 in DC function, suggesting its potential as a biomarker for immunoregulation in HCC. By shaping the TME, MYD88 not only regulates the immune response in HCC but also influences patient clinical outcomes. Both ex vivo and in vivo experiments further validate that MYD88 impacts DC functionality, contributing to variations in HCC progression.

    Keywords: Dendritic Cells, MyD88, Hepatocellular Carcinoma, TME, Immunotherapy

    Received: 02 Jan 2025; Accepted: 12 Mar 2025.

    Copyright: © 2025 Liu, Zhu, Zhang, 朱, He, Yao, Song and Zhang. 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: Xue Zhang, Department of Breast, Renmin Hospital of Wuhan University, Wuhan, 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.

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