ArticleNeurochemical research2025
TSPAN31 Activates EMT Through the PI3 K/AKT Signaling Pathway to Promote Glioma Progression.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- CTGF: The remodeler of the tumor immune microenvironment (Review).Oncology reports · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
As the most malignant primary intracranial tumor, glioma progression has been associated with tetraspanins (TSPANs), a conserved family of transmembrane proteins regulating critical cellular processes including adhesion, proliferation, differentiation, and metastasis. Among TSPAN members, TSPAN31 emerges as a potential oncogene implicated in multiple malignancies. The epithelial-mesenchymal transition (EMT), characterized by enhanced invasiveness and biomarker alterations, represents a pivotal mechanism driving tumor metastasis. Concurrently, the PI3K/AKT pathway, a master regulator of cellular homeostasis, significantly influences oncogenesis and therapeutic resistance. Pan-cancer analysis was performed to evaluate TSPAN31's prognostic value through Kaplan-Meier survival curves and ROC analysis. TSPAN31 expression in glioma tissues and cell lines was quantified via Western blot and qRT-PCR. Functional assessments included CCK-8, EdU incorporation, colony formation, and xenograft models for proliferation analysis, complemented by flow cytometry for apoptosis detection. Transwell and wound healing assays evaluated migratory/invasive capacities. Tumor microenvironment and immune infiltration patterns were analyzed using bioinformatics. Mechanistic investigations employed KEGG pathway enrichment and phosphoprotein profiling of PI3K/AKT signaling. Pharmacological rescue experiments utilized SC79, a PI3K/AKT activator. TSPAN31 exhibited significant upregulation in glioma specimens and cell lines, correlating with poor clinical prognosis. Its knockdown suppressed proliferation, migration, invasion, and xenograft growth, while promoting apoptosis. TSPAN31 depletion attenuated EMT progression and reduced immunosuppressive cell infiltration. Pathway analysis revealed predominant PI3K/AKT pathway association. Silencing TSPAN31 specifically decreased phosphorylated PI3K and AKT without altering total protein levels. SC79 treatment reversed TSPAN31 knockdown effects, restoring malignant phenotypes and EMT marker expression (N-cadherin, E-cadherin). TSPAN31 drives glioma progression by activating EMT through PI3K/AKT signaling, establishing its dual role as a prognostic biomarker and therapeutic target. These findings provide mechanistic insights for developing TSPAN31-directed therapies in glioma management.
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Registered trials
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