Evidence map›Paper›PMID 40196847›Full record

ArticleFrontiers in cell and developmental biology2025

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

Zheming Liu, Hengbo Zhu, Fengxia Zhang, Wenting Huang, Shipeng Zhu, Songjiang He, Yi Yao, Qibin Song, Xue Zhang

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Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Zheming Liu *Cancer Center, Renmin Hospital of Wuhan University, Wuhan, China.
Hengbo Zhu *Department of Pediatrics, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China.
Fengxia Zhang *Department of Rehabilitation Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
Wenting HuangDepartment of Pathology, Renmin Hospital of Wuhan University, Wuhan, China.
Shipeng ZhuCancer Center, Renmin Hospital of Wuhan University, Wuhan, China.
Songjiang HeCancer Center, Renmin Hospital of Wuhan University, Wuhan, China.
Yi YaoCancer Center, Renmin Hospital of Wuhan University, Wuhan, China.
Qibin SongCancer Center, Renmin Hospital of Wuhan University, Wuhan, China.
Xue ZhangDepartment of Breast, Renmin Hospital of Wuhan University, Wuhan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: 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. Methods: RNA-sequencing data retrieved from the TCGA and GEO databases were utilized for both the training and validation of our signature. Single-cell RNA transcriptome data from GEO were analyzed to investigate the correlation among subclusters of T cells, myeloid cells, and dendritic cells (DCs) within the HCC tumor microenvironment (TME). A combination of bioinformatics and machine learning approaches was employed to perform statistical analyses.Additionally, flow cytometry was conducted to quantify T cell subtypes and assess biomarker expression in DCs. A BALB/c-derived xenograft mouse model was established to evaluate the functional role of MyD88 in tumor progression and immunotherapy response. Furthermore, immunohistochemical (IHC) staining was performed to reassess the biological effects of MyD88 in HCC patients undergoing immune checkpoint inhibitor (ICI) therapy. Results: 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 Discussion: 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

Indexed as

dendritic cellshepatocellular carcinomaimmunotherapyMyD88TME

Identifiers

PMID40196847
PMCPMC11973264

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.