ArticleCancer medicine2025
GABRP Mediates GABA-A Receptor to Shape Tumor Immunosuppressive Microenvironment and Promote Tumor Immune Escape and Corresponding Targeted Therapy.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Neural-tumor interactions: bidirectional regulatory mechanisms and nervous system-targeted tumor therapeutic strategies.Biomarker research · 2026Review
- Neural regulation of cancer: from synaptic integration to neuro-immune regulation.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Metabolic Reprogramming and Neurotransmitter Signaling Co-Option in the Glioma Immune Microenvironment: Dual-Axis Regulation of Immunosuppression.Biomolecules · 2026Review
- Neurotransmitters and Immunity: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Adoptive cellular therapy prevents reconstitution of myeloid-derived suppressor cells in the glioma tumor microenvironment.Neuro-oncology advancesArticle
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Authors and funding
10 authors.
Funding
Abstract
backgroundTumor immune evasion mediated by the immunosuppressive tumor microenvironment (TME) remains a major obstacle in cancer therapy. The γ-aminobutyric acid receptor π subunit (GABRP) is aberrantly expressed in cancers, but its role in immune evasion is poorly defined.
objectiveTo elucidate the mechanism of GABRP-driven TME remodeling and evaluate its therapeutic potential. MATERIALS AND
methodsPan-cancer bioinformatics analysis (TCGA, GEPIA2, cBioPortal) assessed GABRP expression, survival associations, and immune infiltration across 33 cancers. Functional studies included GABRP knockdown in glioma cells (U87/U251) via lentiviral RNAi, proliferation/migration assays (CCK-8, scratch test), and pathway analysis. Subcutaneous xenografts in BALB/c-nu mice evaluated the GABA_A inhibitor Amentoflavone. Immune profiling utilized ssGSEA and TIMER.
resultsGABRP was overexpressed in gliomas and other cancers (breast, gastric), correlating with poor prognosis (HR = 1.8, p = 0.008) and enriched immunosuppressive cells (Tregs, M2 macrophages). Knockdown suppressed proliferation (IC50↓42%), migration (> 50% delay, p < 0.01), and PI3K/AKT signaling. Amentoflavone reduced tumor volume by 68% (p < 0.001) and reversed GABA-mediated T cell inhibition. DISCUSSION: GABRP promotes immune evasion via GABA overproduction, recruiting Tregs/M2 macrophages to establish an immunosuppressive TME. Targeting GABRP or GABA signaling (e.g., Amentoflavone) restores antitumor immunity. Limitations include cohort size and tissue-specific heterogeneity.
conclusionGABRP is a key regulator of tumor immunosuppression. Dual strategies-blocking GABRP expression or GABA signaling-offer novel therapeutic avenues. Clinical validation is needed to advance precision oncology.
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