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Updated: Jun 14, 2026
Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma
Yona Kim1,2, Ji Hyeon You1,3, Yeonjoo Ryu1,2
1Department of Neurosurgery, Cancer Research Institute and Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, Korea.
Abstract:
Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly understood. In this study, we elucidate the role of the RNA-binding protein ELAVL2 in regulating aggressive MES transformation in GBM. We found that ELAVL2 is most frequently deleted in GBM compared to other cancers and associated with distinct clinical and molecular features. Transcriptomic analysis revealed that ELAVL2-mediated alterations correspond to specific GBM subtype signatures. Notably, ELAVL2 expression negatively correlated with epithelial-to-mesenchymal transition (EMT)-related genes, and its loss promoted MES process and chemo-resistance in GBM cells, whereas ELAVL2 overexpression exerted the opposite effect. Further investigation via tissue microarray analysis demonstrated that high ELAVL2 protein expression confers a favorable survival outcome in GBM patients. Mechanistically, ELAVL2 was shown to directly bind to the transcripts of EMT-inhibitory molecules, SH3GL3 and DNM3, modulating their mRNA stability, potentially through an m6A-dependent mechanism. In summary, our findings identify ELAVL2 as a critical tumor suppressor and mRNA stabilizer that regulates MES transition in GBM, underscoring its role in transcriptomic plasticity and glioma progression.
Insights
The RNA-binding protein ELAVL2 acts as a tumor suppressor in glioblastoma (GBM). Loss of ELAVL2 promotes aggressive cancer traits and chemo-resistance, while its presence improves patient survival.
Area of Science:
- Neuro-oncology
- Molecular biology
- Cancer research
Background:
- Glioblastoma (GBM) is an aggressive brain cancer characterized by heterogeneity and plasticity.
- Mesenchymal (MES) transition is a key driver of GBM aggressiveness and treatment resistance.
- Regulatory mechanisms of GBM plasticity, especially MES transition, are not fully understood.
Purpose of the Study:
- To investigate the role of RNA-binding protein ELAVL2 in regulating mesenchymal transition in glioblastoma.
- To understand the clinical and molecular implications of ELAVL2 alterations in GBM.
Main Methods:
- Transcriptomic analysis to assess ELAVL2-mediated gene expression changes.
- Functional assays in GBM cells to evaluate the impact of ELAVL2 expression on MES transition and chemo-resistance.
- Tissue microarray analysis to correlate ELAVL2 protein levels with patient survival.
- RNA immunoprecipitation assays to identify direct targets of ELAVL2.
Main Results:
- ELAVL2 is frequently deleted in GBM and associated with distinct clinical features.
- ELAVL2 expression negatively correlates with epithelial-to-mesenchymal transition (EMT) genes; its loss promotes MES transition and chemo-resistance.
- High ELAVL2 protein expression in patients predicts favorable survival outcomes.
- ELAVL2 directly binds to SH3GL3 and DNM3 transcripts, stabilizing them potentially via an m6A-dependent mechanism.
Conclusions:
- ELAVL2 functions as a critical tumor suppressor in glioblastoma.
- ELAVL2 regulates transcriptomic plasticity and mesenchymal transition in GBM by stabilizing specific mRNA targets.
- ELAVL2 is a potential therapeutic target for improving glioblastoma treatment outcomes.
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