ReviewOncotarget2018
Protein arginine methyltransferase 5 (PRMT5) dysregulation in cancer.
Review in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
68 citing papers in PubMed, 118 citations in OpenAlex.
- PRMT5 encourages cell migration and metastasis of tongue squamous cell carcinoma through methylating ΔNp63α.Cell death and differentiation · 2026Article
- PRMT5 in mitochondria regulates mtDNA stability through TFAM arginine methylation.Nature communications · 2026Article
- A Further Case for Targeting PRMT5 and the ERK1/2 and PI3K Pathways in CRC.International journal of molecular sciences · 2025Article
- Congenital heart disease missense mutations in the TBX5 DNA-binding domain alter thermal stability and DNA-binding affinity.G3 (Bethesda, Md.) · 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
- Emerging roles of protein arginine methyltransferase in multiple myeloma.Molecular therapy. Oncology · 2025Review
- Current landscape and future directions of therapeutic approaches for adenoid cystic carcinoma of the salivary glands (Review).Oncology letters · 2025Review
- TBL2 Promotes Tumorigenesis via PRMT5/WDR77-Mediated AKT Activation in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- CD38 symmetric dimethyl site R58 promotes malignant tumor cell immune escape by regulating the cAMP-GSK3β-PD-L1 axis.Heliyon · 2024Article
- PRMT1 promotes epigenetic reprogramming associated with acquired chemoresistance in pancreatic cancer.Cell reports · 2024Article
- PRMT5-mediated methylation of STAT3 is required for lung cancer stem cell maintenance and tumour growth.Communications biology · 2024Article
- Resistance to PRMT5-targeted therapy in mantle cell lymphoma.Blood advances · 2024Article
- Review
- PRMT5 participates in B cell overactivation in patients with primary Sjogren's syndrome (pSS) through RSAD2-mediated NF-κB signaling.Immunity, inflammation and disease · 2023Article
- Enzyme-mediated depletion of methylthioadenosine restores T cell function in MTAP-deficient tumors and reverses immunotherapy resistance.Cancer cell · 2023Article
- PRMT5 triggers glucocorticoid-induced cell migration in triple-negative breast cancer.Life science alliance · 2023Article
- Autophagy dictates sensitivity to PRMT5 inhibitor in breast cancer.Scientific reports · 2023Article
- A type II protein arginine methyltransferase regulates merozoite invasion in Plasmodium falciparum.Communications biology · 2023Article
- The cancer testis antigen TDRD1 regulates prostate cancer proliferation by associating with the snRNP biogenesis machinery.Oncogene · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein arginine methyltransferases (PRMTs) are known for their ability to catalyze methylation of specific arginine residues in a wide variety of cellular proteins, which are involved in a plethora of processes including signal transduction, transcription, and more recently DNA recombination. All members of the PRMT family can be grouped into three main classes depending on the type of methylation they catalyze. Type I PRMTs induce monomethylation and asymmetric dimethylation, while type II PRMTs catalyze monomethylation and symmetric dimethylation of specific arginine residues. In contrast, type III PRMTs carry out only monomethylation of arginine residues. In this review, we will focus on PRMT5, a type II PRMT essential for viability and normal development, which has been shown to be overexpressed in a wide variety of cancer cell types, owing it to the crucial role it plays in controlling key growth regulatory pathways. Furthermore, the role of PRMT5 in regulating expression and stability of key transcription factors that control normal stem cell function as well as cancer stem cell renewal will be discussed. We will review recent work that shows that through its ability to methylate various cellular proteins, PRMT5 functions as a master epigenetic regulator essential for growth and development, and we will highlight studies that have examined its dysregulation and the effects of its inhibition on cancer cell growth.
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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.