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SLC10A3 drives glioblastoma progression by remodeling the immunosuppressive microenvironment and promoting M2 macrophage migration.

Overview

Authors: Shuhui Chen1,2, Daogang Qin3, Hanyang Lin1, Taohui Ding4, Wei Liu1, Ziqi Yan1, Lingting Wang1, Bo Kou1
  1. Department of Otorhinolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China
  2. Department of Comprehensive Radiation Oncology, Jiangxi Key Laboratory of oncology, Jiangxi Cancer Hospital, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Cancer Institute, Nanchang, Jiangxi, China
  3. Department of science and education, The First People’s Hospital of Jiangxia District, Hubei University of Medicine, Shiyan, Hubei, China
  4. Department of Thoracic Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China
Journal: Frontiers in oncology, volume 16, article 1742452
Dates: received 11 November 2025; accepted 10 April 2026; published online 13 May 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.3389/fonc.2026.1742452 · PMID 42211491 · PMCID PMC13212135 · OpenAlex W7160987148
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: genetics / omics (modality), other condition (population), clinical / translational (subfield)
Methods: Statistics, Smoothing, state filtering, decompositions, Connectivity, Machine learning
Keywords: glioblastoma, immunosuppression, M2 macrophages, SLC10A3, therapeutic target, tumor microenvironment
Topic: Immune cells in cancer (Immunology, Immunology and Microbiology), according to OpenAlex
Citations: not cited yet (Europe PMC); 42 references in the paper

Abstract

Introduction: Glioblastoma (GBM) is an aggressive brain tumor with poor prognosis, limited therapeutic options, and a highly immunosuppressive microenvironment. This study investigated the clinical significance and biological role of SLC10A3 in GBM progression and immune evasion.

Methods: Bulk transcriptomic data from TCGA and CGGA cohorts were analyzed to assess SLC10A3 expression and prognostic value. Functional enrichment, single-cell RNA sequencing, and cell–cell communication analyses were performed to explore SLC10A3-related pathways and cellular distribution. In vitro and in vivo experiments were conducted to evaluate the effects of SLC10A3 knockdown on GBM malignant phenotypes and macrophage recruitment.

Results: SLC10A3 was significantly overexpressed in GBM and associated with poor prognosis. Enrichment analyses linked SLC10A3 to PI3K-Akt, NF-κB, HIF-1 signaling, macrophage infiltration, and T-cell suppression. Single-cell analysis showed SLC10A3 enrichment in tumor-associated astrocytes and macrophages, with enhanced astrocyte–macrophage crosstalk through MIF, MDK, and extracellular matrix remodeling pathways. SLC10A3 knockdown inhibited GBM cell proliferation, migration, and invasion, induced cell cycle arrest and apoptosis, reduced M2 macrophage migration, and suppressed xenograft tumor growth.

Discussion: SLC10A3 may promote GBM aggressiveness and immune evasion by regulating malignant phenotypes and macrophage-associated immunosuppression, suggesting its potential as a therapeutic target for GBM.

Reproduced under the paper's license (CC BY), from the paper cited above.

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Data availability statement

The original contributions presented in the study are included in the article/Supplementary Material. Further inquiries can be directed to the corresponding authors.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 28 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 8 authors, 6 keywords, 42 references.

Cite

This paper

Chen, S., Qin, D., Lin, H., Ding, T., Liu, W., Yan, Z., Wang, L., & Kou, B. (2026). SLC10A3 drives glioblastoma progression by remodeling the immunosuppressive microenvironment and promoting M2 macrophage migration. Frontiers in oncology, 16, 1742452. https://doi.org/10.3389/fonc.2026.1742452

BibTeX

@article{chen2026slc10a3,
author = {Chen, Shuhui and Qin, Daogang and Lin, Hanyang and Ding, Taohui and Liu, Wei and Yan, Ziqi and Wang, Lingting and Kou, Bo},
title = {{SLC10A3 drives glioblastoma progression by remodeling the immunosuppressive microenvironment and promoting M2 macrophage migration}},
journal = {Frontiers in oncology},
year = {2026},
month = may,
volume = {16},
pages = {1742452},
publisher = {Frontiers Media SA},
issn = {2234-943X},
doi = {10.3389/fonc.2026.1742452},
url = {https://doi.org/10.3389/fonc.2026.1742452},
pmid = {42211491},
pmcid = {PMC13212135}
}

RIS

TY - JOUR
AU - Chen, Shuhui
AU - Qin, Daogang
AU - Lin, Hanyang
AU - Ding, Taohui
AU - Liu, Wei
AU - Yan, Ziqi
AU - Wang, Lingting
AU - Kou, Bo
TI - SLC10A3 drives glioblastoma progression by remodeling the immunosuppressive microenvironment and promoting M2 macrophage migration
T2 - Frontiers in oncology
J2 - Front Oncol
PY - 2026
DA - 2026/05/13
VL - 16
SP - 1742452
SN - 2234-943X
PB - Frontiers Media SA
DO - 10.3389/fonc.2026.1742452
UR - https://doi.org/10.3389/fonc.2026.1742452
LA - en
ER -

CSL-JSON

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"author": [
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"given": "Shuhui"
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"DOI": "10.3389/fonc.2026.1742452",
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"ISSN": "2234-943X",
"publisher": "Frontiers Media SA",
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"language": "en",
"issued": {
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