ArticleCancer research2014
Genetic validation of the protein arginine methyltransferase PRMT5 as a candidate therapeutic target in glioblastoma.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.
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Who cites it
94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 183 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- Clinicopathological and Prognostic Significance of PRMT5 in Cancers: A System Review and Meta-Analysis.Cancer control : journal of the Moffitt Cancer CenterPooled it
- PRMT5 as a Key Driver of Stemness and Metastatic Potential in Triple-Negative Breast Cancer.Biomolecules · 2026Review
- Identification of METTL3 and PRMT5 as an oncogenic pair for the prognosis and therapeutic targets of colorectal cancer subtype.Clinical epigenetics · 2026Article
- PRMT5 inhibition impairs Fanconi Anemia pathway-mediated homologous recombination and enhances the antitumor efficacy of Temozolomide in glioblastoma.Cell death & disease · 2026Article
- Protein arginine methyltransferase 5 as a novel therapeutic target in solid tumors.Genes & diseases · 2026Review
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- The Role of Protein Arginine Methylation as a Post-Translational Modification in Cellular Homeostasis and Disease.Biology · 2025Review
- Exploiting Synthetic Lethality of PRMT5 for Precision Treatment of MTAP-Deficient Glioblastoma.International journal of translational medicine (Basel, Switzerland) · 2025Article
- Combined inhibition by PRMT5 and MAT2A demonstrates a strong synthetic lethality in MTAP homozygous-deficient glioma models.Cell death discovery · 2025Article
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- Protein Arginine Methyltransferases from Regulatory Function to Clinical Implication in Central Nervous System.Cellular and molecular neurobiology · 2025Review
- PRMT5 inhibition sensitizes glioblastoma tumor models to temozolomide.Research square · 2025Article
- Protein arginine methyltransferases as regulators of cellular stress.Experimental neurology · 2025Review
- Basic Epigenetic Mechanisms.Sub-cellular biochemistry · 2025Review
- Inhibitory Effect of PRMT5/MTA Inhibitor on MTAP-Deficient Glioma May Be Influenced by Surrounding Normal Cells.Cancer medicine · 2024Article
- PRMT5/WDR77 Enhances the Proliferation of Squamous Cell Carcinoma via the ΔNp63α-p21 Axis.Cancers · 2024Article
- Targeting PRMT5 enhances the radiosensitivity of tumor cells grown in vitro and in vivo.Scientific reports · 2024Article
- PRMT6 facilitates EZH2 protein stability by inhibiting TRAF6-mediated ubiquitination degradation to promote glioblastoma cell invasion and migration.Cell death & disease · 2024Article
- Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
35 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma is the most common and aggressive histologic subtype of brain cancer with poor outcomes and limited treatment options. Here, we report the selective overexpression of the protein arginine methyltransferase PRMT5 as a novel candidate theranostic target in this disease. PRMT5 silences the transcription of regulatory genes by catalyzing symmetric dimethylation of arginine residues on histone tails. PRMT5 overexpression in patient-derived primary tumors and cell lines correlated with cell line growth rate and inversely with overall patient survival. Genetic attenuation of PRMT5 led to cell-cycle arrest, apoptosis, and loss of cell migratory activity. Cell death was p53-independent but caspase-dependent and enhanced with temozolomide, a chemotherapeutic agent used as a present standard of care. Global gene profiling and chromatin immunoprecipitation identified the tumor suppressor ST7 as a key gene silenced by PRMT5. Diminished ST7 expression was associated with reduced patient survival. PRMT5 attenuation limited PRMT5 recruitment to the ST7 promoter, led to restored expression of ST7 and cell growth inhibition. Finally, PRMT5 attenuation enhanced glioblastoma cell survival in a mouse xenograft model of aggressive glioblastoma. Together, our findings defined PRMT5 as a candidate prognostic factor and therapeutic target in glioblastoma, offering a preclinical justification for targeting PRMT5-driven oncogenic pathways in this deadly disease.
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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.