ArticleJournal of neuro-oncology2026
Disrupting Akt-Wnt/β-catenin signaling suppresses glioblastoma stem cell growth and tumor progression in immunocompetent mice.
Article in Journal of neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeGlioblastoma (GBM) is an aggressive primary malignant brain tumor in adults with a median patient survival of 12-18 months post-diagnosis, and no effective treatments, to date. The PI3K/Akt and Wnt/β-catenin signaling pathways promote GBM cell growth, survival, invasiveness and therapeutic resistance. We hypothesize that inhibiting Akt and β-catenin, which are central regulatory proteins of the PI3K/Akt and Wnt/β-catenin pathway, will suppress GBM growth and progression.
methodsMouse glioma cells (CT-2A) and human patient-derived glioma stem cells (N08-30) were treated with pan-Akt inhibitor, MK-2206, or β-catenin inhibitor, iCRT3, to evaluate effects on cell viability, apoptosis, β-catenin transcriptional activity, and Wnt gene and protein expression, in vitro. Luciferase-expressing CT-2A cells were inoculatedintracraniallyin immunocompetent C57BL/6J mice to assess the impact of MK-2206 treatment on tumor progression using bioluminescence imaging and immunohistochemistry.
resultsIn vitro studies demonstrate that MK-2206, a pan-Akt inhibitor, effectively reduced cell viability, induced apoptosis, and inhibited β-catenin activity; consistently outperforming iCRT3, a β-catenin-TCF interaction inhibitor, in CT-2A mouse glioma cells, and N08-30 human glioma stem cells. MK-2206 significantly suppressed tumor growth in vivo, and reduced expression of phosphorylated Akt and GSK-3β in tumor tissues, confirming disruption of the Akt and Wnt/β-catenin signaling axis.
conclusionIn summary, MK-2206 outperformed iCRT3 efficacy in vitro, and suppressed GBM progression, in vivo. These findings suggest that Akt inhibition via MK-2206 may offer a promising therapeutic strategy for treating GBM, characterized by dysregulation of PI3K/Akt or Wnt/β-catenin pathways.
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