ArticleCytoJournal2026
Gamma-aminobutyric acid affects the tumor microenvironment and angiogenesis, promoting breast cancer progression.
Article in CytoJournal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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3 authors.
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Abstract
Objective: Breast cancer (BC) is one of the most common malignant tumors among women. Gamma-aminobutyric acid (GABA) is abnormally expressed in various cancers, but its effect on BC remains unclear. This study aims to explore the expression changes of glutamic acid decarboxylase 1 (GAD1) in BC and its mechanism of promoting tumor occurrence and development by regulating GABA synthesis. Material and Methods: GAD1 expression and GABA levels in BC cells (MDA-MB-231) and normal breast epithelial cells (MCF-10A) were measured. GAD1 overexpression and knockdown cell lines were constructed to evaluate the changes in GABA levels and their effects on cell proliferation and invasion ability. Macrophage M2 polarization and protumor factor levels were analyzed by coculturing tumor cells with macrophages. Cell activity was detected by coculturing with CD8 Results: GAD1 expression and GABA level in MDA-MB-231 cells were significantly higher than those in normal cells ( Conclusion: GAD1 is highly expressed in BC. Increasing GABA synthesis promotes tumor cell proliferation and metastasis, regulates the immune microenvironment toward immunosuppression, and enhances tumor angiogenesis. This work reveals the crucial role of the GAD1-GABA pathway in BC and provides a potential therapeutic target for this disease.
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