ArticleNPJ precision oncology2024
ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma.
Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- RNA Expression Signatures in Glioblastoma: A Systematic Review of Tumour Biology and Therapeutic Targets.Oncology research · 2025Pooled it
- Tumor Electric Field Therapy Inhibits Epithelial-Mesenchymal Transition, Invasion, and Migration of Glioblastoma by Targeting the c-FOS/CXCL14 Axis.CNS neuroscience & therapeutics · 2026Article
- GATOR1 complex controls cisplatin sensitivity.Cell death & disease · 2025Article
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- YTHDF2 regulates the adriamycin (ADM) resistance in NKTCL by modulating the m6A modification of SLC16A9.Translational oncology · 2025Article
- Inhibition of FOXM1 Leads to Suppression of Cell Proliferation, Migration, and Invasion Through AXL/eEF2 Kinase Signaling and Induces Apoptosis and Ferroptosis in GBM Cells.International journal of molecular sciences · 2025Article
- Does side matter? Deciphering mechanisms that underpin side-dependent pathogenesis and therapy response in colorectal cancer.Molecular cancer · 2025Review
- Identification of novel diagnostic and prognostic microRNAs in sarcoma on TCGA dataset: bioinformatics and machine learning approach.Scientific reports · 2025Article
- A Systematic Quantitative Approach to Rational Drug Design and the Discovery of Novel Human Antigen R (HuR) Inhibitors.Anti-cancer agents in medicinal chemistry · 2025Article
- RNA Binding Proteins are Pivotal Regulators of Cancer Radioresistance and Potential Targets for Preventing Tumor Recurrence.Current radiopharmaceuticals · 2025Review
- Treatment challenges in glioblastoma: a case report.Frontiers in oncology · 2025Article
- Protein-RNA interaction dynamics reveal key regulators of oncogenic KRAS-driven cancers.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
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.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.