ArticleOncogene2025
PRMT5-regulated splicing of DNA repair genes drives chemoresistance in breast cancer stem cells.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Dietary sulforaphane in cancer chemoprevention: epigenetic regulation and PRMT5-MEP50 complex inhibition-a systematic review.Frontiers in pharmacology · 2026Pooled it
- Targeting PRMT5 Inhibitor-Induced Adaptation in Pancreatic Cancer with the RBM39 Degrader Indisulam.Cancer research communications · 2026Article
- PRMT5-mediated intron retention triggers innate and adaptive immunity against cancer.EMBO molecular medicine · 2026Article
- PRMT5 as a Key Driver of Stemness and Metastatic Potential in Triple-Negative Breast Cancer.Biomolecules · 2026Review
- Emerging role of protein arginine methyltransferase 5 in gastrointestinal cancer (Review).Oncology letters · 2026Review
- PRMT5 inhibition impairs Fanconi Anemia pathway-mediated homologous recombination and enhances the antitumor efficacy of Temozolomide in glioblastoma.Cell death & disease · 2026Article
- Disulfiram metabolite Cu(DDC)EBioMedicine · 2026Article
- PRMT5 inhibition triggers functional ATM deficiency and sensitizes pancreatic cancer to CHK1 blockade.Frontiers in cell and developmental biology · 2026Article
- Replication-associated base excision repair/single-strand break repair regulates PARG inhibitor response via the PRMT1/PRMT5/ATR axis.NAR cancer · 2025Article
- USP30-AS1 Dictates Breast Cancer Cell Fate and Chemoresistance via a miR-3646/FZD7/Wnt/β-Catenin Circuit.Current issues in molecular biology · 2025Article
- Protein arginine methyltransferase 5 sustains Tip60-EP400 complex via SRSF1 in Merkel cell carcinoma.Life science alliance · 2025Article
- EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025Review
- PRMT5 activity sustains histone production to maintain genome integrity.bioRxiv : the preprint server for biology · 2025Article
- Protein Arginine Methyltransferases from Regulatory Function to Clinical Implication in Central Nervous System.Cellular and molecular neurobiology · 2025Review
- Editorial: The emerging role of protein methylation/demethylation modification in disease and homeostasis.Frontiers in molecular biosciences · 2025Article
- Harnessing the interaction between redox signaling and senescence to restrain tumor drug resistance.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Breast cancer stem cells (BCSCs) are a rare cell population that is responsible for tumour initiation, metastasis and chemoresistance. Despite this, the mechanism by which BCSCs withstand genotoxic stress is largely unknown. Here, we uncover a pivotal role for the arginine methyltransferase PRMT5 in mediating BCSC chemoresistance by modulating DNA repair efficiency. Mechanistically, we identify PRMT5 as a major regulator of DNA damage response (DDR) gene splicing in BCSCs, particularly those integral to the Fanconi Anaemia and homologous recombination pathways, with PRMT5 inhibition synergising with chemotherapy to promote BCSC apoptosis. A comparison of BCSCs and their bulk cell progeny identified some shared (ATM, DDX11, EXO1, FAN1, SLX4) but many unique (ATR, RAD17, RAD51D, RUVBL1) PRMT5-dependent alternative DDR splicing events. Surprisingly, these skipped exons and retained intron events rarely lead to substantial gene expression repression, suggesting that PRMT5 inhibition predominantly results in nuclear detention of intron-containing transcripts and the production of non-canonical isoforms with compromised protein function. Since many genes within the same DDR pathway undergo deregulated splicing, this study thus reveals additional points of vulnerability and alternative combination drug strategies that could improve the therapeutic efficacy of PRMT5 inhibitors to promote BCSC eradication.
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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.