ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
GNE-317 Reverses MSN-Mediated Proneural-to-Mesenchymal Transition and Suppresses Chemoradiotherapy Resistance in Glioblastoma via PI3K/mTOR.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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.
- ASPDH inhibits the proliferation, migration, and invasion of liver cancer cells by regulating lactate metabolism and the NF-κB/PD-L1 pathway.Clinics (Sao Paulo, Brazil) · 2026Article
- Esketamine Enhances the Chemosensitivity of Colorectal Adenocarcinoma Cells to 5-Fluorouracil via AMPK/mTOR/HMMR Signaling Pathway.Oncology research · 2026Article
- Unravelling genomic differences in cerebrospinal fluid: patients with lung cancer with combined brain parenchymal and meningeal metastasis versus exclusive meningeal metastasis.Journal of neuro-oncology · 2025Article
- Melatonin Synergises the Chemotherapeutic Effect of Temozolomide in Glioblastoma by Suppressing NF-κB/COX-2 Signalling Pathways.Journal of cellular and molecular medicine · 2025Article
- GNE-317 Reverses MSN-Mediated Proneural-to-Mesenchymal Transition and Suppresses Chemoradiotherapy Resistance in Glioblastoma via PI3K/mTOR.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
Glioblastoma (GBM) resistance to chemoradiotherapy is a major factor contributing to poor treatment outcomes. This resistance markedly affects the effectiveness of surgery combined with chemoradiotherapy and leads to post-surgical tumor recurrence. Therefore, exploring the mechanisms underlying chemoradiotherapy resistance in GBM is crucial for understanding its progression and improving therapeutic options. This study found that moesin (MSN) acts as a key promotor of chemoradiotherapy resistance in glioma stem cells (GSCs), enhancing their proliferation and stemness maintenance. Mechanistically, MSN activates the downstream PI3K/mTOR signaling pathway, driving the proneural-to-mesenchymal transition (PMT) in GSCs. This process enhances the repair of DNA damage caused by radiotherapy (RT) and temozolomide (TMZ), thereby increasing the resistance of GSCs to chemoradiotherapy. Additionally, GNE-317, a small molecule drug capable of crossing the blood-brain barrier, specifically inhibits MSN and suppresses the activation of downstream PI3K/mTOR signaling. Importantly, the combination of GNE-317 with RT and TMZ exhibits a strong synergistic effect both in vivo and in vitro, achieving better efficacy compared to the traditional combination of RT and TMZ. This study not only advances understanding of the mechanisms underlying chemoradiotherapy resistance in GBM but also provides a promising new approach for enhancing treatment outcomes.
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