ArticleCancer science2012
Protein arginine methyltransferase 5 is a potential oncoprotein that upregulates G1 cyclins/cyclin-dependent kinases and the phosphoinositide 3-kinase/AKT signaling cascade.
Article in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
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Who cites it
128 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.
- Drug repositioning discovery for early- and late-stage non-small-cell lung cancer.BioMed research international · 2014Pooled it
- Targeting PRMTs with small-molecule inhibitors: a comprehensive review.RSC medicinal chemistry · 2026Review
- Emerging role of protein arginine methyltransferase 5 in gastrointestinal cancer (Review).Oncology letters · 2026Review
- BUD23 is associated with malignancy and correlates with immune infiltration in NSCLC.Oncology letters · 2026Article
- Multifaceted bioinformatic analysis uncover links m5C-related ferroptosis gene SLC2A1 to prognosis and immune infiltration in lung adenocarcinoma.Discover oncology · 2026Article
- Dynamic regulation of histone arginine methylation in anoxic freshwater turtles.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2026Article
- Protein Arginine Methyltransferases in γ-Globin Regulation and Sickle Cell Disease: Emerging Connections to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Integrated Network Analysis Reveals a Directly Regulatory Network of FOXM1 Associated With the Cell Cycle in Lung Adenocarcinoma.Bioinformatics and biology insights · 2026Article
- A novel cuproptosis-related prognostic gene signature and validation of differential expression in colon cancer.Discover oncology · 2025Article
- PRMT5 Inhibition as a Potential Strategy for KRAS Mutant CRC: Downstream Mediators of the PRMT5-KRAS Crosstalk.Current issues in molecular biology · 2025Article
- Current and Emerging Therapies for Targeting Protein Arginine Methyltransferases (PRMTs) in Cancer.International journal of molecular sciences · 2025Review
- MicroRNA-100-5p Exacerbates Myocardial Ischemia-Reperfusion Injury Through Downregulation of PRMT5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Identification of a Selective Cell-Active Inhibitor of Protein Arginine Methyltransferase 5 (PRMT5) for the Treatment of Prostate Cancer by Structure-Based Virtual Screening.Chemical biology & drug design · 2025Article
- A Novel Neutrophil Extracellular Trap Signature Predicts Patient Chemotherapy Resistance and Prognosis in Lung Adenocarcinoma.Molecular biotechnology · 2025Article
- Applications of gene pair methods in clinical research: advancing precision medicine.Molecular biomedicine · 2025Review
- Low Expression of SCN4B Predicts Poor Prognosis in Non-small Cell Lung Cancer.Current cancer drug targets · 2025Article
- Identification of potential biomarkers for lung cancer using integrated bioinformatics and machine learning approaches.PloS one · 2025Article
- Integration of osimertinib-targeted EGFR gene-associated differential gene expression in constructing a prognostic model for lung adenocarcinoma.Functional & integrative genomics · 2024Article
- Methylation of KSHV vCyclin by PRMT5 contributes to cell cycle progression and cell proliferation.PLoS pathogens · 2024Article
- Article
68 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that PRMT5, a protein arginine methyltransferase, is involved in tumorigenesis. However, no systematic research has demonstrated the cell-transforming activity of PRMT5. We investigated the involvement of PRMT5 in tumor formation. First, we showed that PRMT5 was associated with many human cancers, through statistical analysis of microarray data in the NCBI GEO database. Overexpression of ectopic PRMT5 per se or its specific shRNA enhanced or reduced cell growth under conditions of normal or low concentrations of serum, low cell density, and poor cell attachment. A stable clone that expressed exogenous PRMT5 formed tumors in nude mice, which demonstrated that PRMT5 is a potential oncoprotein. PRMT5 accelerated cell cycle progression through G1 phase and modulated regulators of G1; for example, it upregulated cyclin-dependent kinase (CDK) 4, CDK6, and cyclins D1, D2 and E1, and inactivated retinoblastoma protein (Rb). Moreover, PRMT5 activated phosphoinositide 3-kinase (PI3K)/AKT and suppressed c-Jun N-terminal kinase (JNK)/c-Jun signaling cascades. However, only inhibition of PI3K activity, and not overexpression of JNK, blocked PRMT5-induced cell proliferation. Further analysis of PRMT5 expression in 64 samples of human lung cancer tissues by microarray and western blot analysis revealed a tight association of PRMT5 with lung cancer. Knockdown of PRMT5 retarded cell growth of lung cancer cell lines A549 and H1299. In conclusion, to the best of our knowledge, we have characterized the cell-transforming activity of PRMT5 and delineated its underlying mechanisms for the first time.
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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.