ArticleFrontiers in oncology2026
SLC10A3 drives glioblastoma progression by remodeling the immunosuppressive microenvironment and promoting M2 macrophage migration.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.