ArticleScience advances2025
Pharmacologic degradation of WDR5 suppresses oncogenic activities of SS18::SSX and provides a therapeutic of synovial sarcoma.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- An EZH2-SREBP2 axis promotes cholesterol biosynthesis and represents a noncanonical vulnerability in tumorigenesis.Nature cell biology · 2026Article
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- Advances in targeted therapies for pediatric tumors.Acta pharmacologica Sinica · 2026Article
- Mono-ubiquitination of histone H2A lysine 119 (H2AK119Ub): its multifaceted role in biology and implication in diseases.MedScience · 2026Review
- BAF complex-independent gene activation by SS18::SSX.bioRxiv : the preprint server for biology · 2026Article
- Synovial sarcoma reprograms transcription by GBAF activation of polycomb targets and loss of CBAF enhancers.Nature communications · 2025Article
- Molecular and epigenetic oncogenesis in synovial sarcoma: implications for cancer biology, diagnosis and treatment.Oncogene · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Cancer-causing aberrations recurrently target the chromatic-regulatory factors, leading to epigenetic dysregulation. Almost all patients with synovial sarcoma (SS) carry a characteristic gene fusion, SS18::SSX, which produces a disease-specific oncoprotein that is incorporated into the switch/sucrose non-fermentable (SWI/SNF) chromatin-remodeling complexes and profoundly alters their functionalities. Targeting epigenetic dependency in cancers holds promise for improving current treatment. Leveraging on cancer cell dependency dataset, pharmacological tools, and genomic profiling, we find WDR5, a factor critical for depositing histone H3 lysine 4 (H3K4) methylation, to be an unexplored vulnerability in SS. Mechanistically, WDR5 and SS18::SSX interact and colocalize at oncogenes where WDR5 promotes H3K4 methylation and the chromatin association of SS18::SSX-containing chromatin-remodeling complexes. WDR5 degradation by proteolysis-targeting chimera (PROTAC) not only suppresses the SS18::SSX-related oncogenic programs but additionally causes the ribosomal protein deregulations leading to p53 activation. WDR5-targeted PROTAC suppresses SS growth in vitro and in vivo, providing a promising strategy for the SS treatment.
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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.