ArticleJournal of experimental & clinical cancer research : CR2024
Targeting PRMT5 through PROTAC for the treatment of triple-negative breast cancer.
Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The trial behind it
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Who cites it
24 citing papers in PubMed.
- Targeting PRMTs with small-molecule inhibitors: a comprehensive review.RSC medicinal chemistry · 2026Review
- MTAP Deficiency as a Metabolic Vulnerability in Cancer: Implications for Synthetic Lethal Therapy.Cancer science · 2026Review
- Article
- PROTAC-mediated regulation of programmed cell death: From molecular mechanisms to therapeutic breakthroughs.Innovation (Cambridge (Mass.)) · 2026Review
- PRMT5 as a Key Driver of Stemness and Metastatic Potential in Triple-Negative Breast Cancer.Biomolecules · 2026Review
- MS4322 is a selective protein arginine methyltransferase 5 degrader with antitumor effects in cervical cancer cells.Oncology reports · 2026Article
- Review
- Research Progress of PROTACs in Breast Cancer: Subtype-Oriented Target Landscape, Clinical Stratification Evidence, and Engineering Strategies for Translation.Biomedicines · 2026Review
- Protein arginine methyltransferases in cancer: mechanisms, functions, and therapeutic opportunities.Journal of biomedical science · 2026Review
- Hongwu mixture exerts inhibition on triple-negative breast cancer by regulating SAV1/Hippo signaling through ZNF143.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- PRMT5 encourages cell migration and metastasis of tongue squamous cell carcinoma through methylating ΔNp63α.Cell death and differentiation · 2026Article
- Advances in the Research and Development of Breast Cancer Organoids.Oncology research · 2026Review
- Cracking PRMT5: Mechanistic insights, clinical advances, and AI-driven strategies.Cancer letters · 2025Review
- PH20-modified exosomes loaded curcumin inhibit desmoplastic breast cancer by breaking extracellular matrix barrier and normalizing cancer-associated fibroblasts.Materials today. Bio · 2025Article
- Drug resistance in cancer: molecular mechanisms and emerging treatment strategies.Molecular biomedicine · 2025Review
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025Review
- Therapeutic Targeting of Protein Lysine and Arginine Methyltransferases: Principles and Strategies for Inhibitor Design.International journal of molecular sciences · 2025Review
- Single-cell multi-omics and machine learning for dissecting stemness in cancer.Briefings in bioinformatics · 2025Review
- PRMT1-catalyzed NUSAP1 methylation enhances Notch2 signaling and 5-FU resistance in gastric cancer.Cell death & disease · 2025Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) is currently the most aggressive subtype of breast cancer, characterized by high heterogeneity and strong invasiveness, and currently lacks effective therapies. PRMT5, a type II protein arginine methyltransferase, is upregulated in numerous cancers, including TNBC, and plays a critical role, marked it as an attractive therapeutic target. PROTAC (Proteolysis Targeting Chimeras) is an innovative drug development technology that utilizes the ubiquitin-proteasome system (UPS) to degrade target proteins, which is characterized by higher activity, enhanced safety, lower resistance, and reduced toxicity, offering significant value for clinical translation.
methodsThis study utilizes the PROTAC technology to develop potential degraders targeting PRMT5 in vitro and in vivo.
resultsThrough the design, synthesis and screening of a series of targeted compounds, we identified YZ-836P as an effective compound that exerted cytotoxic effects and reduced the protein levels of PRMT5 and its key downstream target protein KLF5 in TNBC after 48 h. Its efficacy was significantly superior to the PRMT5 PROTAC degraders that had been reported. YZ-836P induced G1 phase cell cycle arrest and significantly induced apoptosis in TNBC cells. Additionally, we demonstrated that YZ-836P promoted the ubiquitination and degradation of PRMT5 in a cereblon (CRBN)-dependent manner. Notably, YZ-836P exhibited pronounced efficacy in inhibiting the growth of TNBC patient-derived organoids and xenografts in nude mice.
conclusionsThese findings position YZ-836P as a promising candidate for advancing treatment modalities for TNBC.
trial registrationEthics Committee of Yunnan Cancer Hospital, KYCS2023-078. Registered 7 June 2023.
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