ArticleNature communications2021
Dual functions of SPOP and ERG dictate androgen therapy responses in prostate cancer.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 43 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- Exploring the biology of metastatic hormone-sensitive prostate cancer: on the road to precision medicine.The Journal of clinical investigation · 2026Review
- Novel intermolecular zinc fingers and redox-driven conformational changes dictate tumor suppressor ZMYND11's role in cooperative recognition of diverse targets.Nucleic acids research · 2026Article
- Intratumoral Androgens and Genetic Variants Driving Therapy Resistance in Prostate Cancer.Research (Washington, D.C.) · 2026Review
- Precision Medicine in Prostate Cancer with a Focus on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis.Nature communications · 2025Article
- Germline-Somatic Liaison Dictates Cancer Subtypes via de novo Steroid Biosynthesis.Cancer discovery · 2025Article
- Harnessing the SPOP E3 Ubiquitin Ligase via a Bridged Proteolysis Targeting Chimera (PROTAC) Strategy for Targeted Protein Degradation.Journal of medicinal chemistry · 2025Article
- Article
- Cul3 substrate adaptor SPOP targets Nup153 for degradation.Molecular biology of the cell · 2025Article
- Prostate Cancer Progression Modeling Provides Insight into Dynamic Molecular Changes Associated with Progressive Disease States.Cancer research communications · 2024Article
- Identification of recurrent BRAF non-V600 mutations in intraductal carcinoma of the prostate in Chinese populations.Neoplasia (New York, N.Y.) · 2024Article
- Inhibition of the proline metabolism rate-limiting enzyme P5CS allows proliferation of glutamine-restricted cancer cells.Nature metabolism · 2023Article
- Identification of bicalutamide resistance-related genes and prognosis prediction in patients with prostate cancer.Frontiers in endocrinology · 2023Article
- Genomic, epigenomic, and transcriptomic signatures of prostate cancer between African American and European American patients.Frontiers in oncology · 2023Review
- Molecular classifications of prostate cancer: basis for individualized risk stratification and precision therapy.Annals of medicine · 2023Review
- Race and prostate cancer: genomic landscape.Nature reviews. Urology · 2022Review
- Interplay of Developmental Hippo-Notch Signaling Pathways with the DNA Damage Response in Prostate Cancer.Cells · 2022Review
- ERK1/2 inhibits Cullin 3/SPOP-mediated PrLZ ubiquitination and degradation to modulate prostate cancer progression.Cell death and differentiation · 2022Article
Corrections and comments
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Authors and funding
32 authors at 6 institutions in 4 countries.
Funding
Abstract
Driver genes with a mutually exclusive mutation pattern across tumor genomes are thought to have overlapping roles in tumorigenesis. In contrast, we show here that mutually exclusive prostate cancer driver alterations involving the ERG transcription factor and the ubiquitin ligase adaptor SPOP are synthetic sick. At the molecular level, the incompatible cancer pathways are driven by opposing functions in SPOP. ERG upregulates wild type SPOP to dampen androgen receptor (AR) signaling and sustain ERG activity through degradation of the bromodomain histone reader ZMYND11. Conversely, SPOP-mutant tumors stabilize ZMYND11 to repress ERG-function and enable oncogenic androgen receptor signaling. This dichotomy regulates the response to therapeutic interventions in the AR pathway. While mutant SPOP renders tumor cells susceptible to androgen deprivation therapies, ERG promotes sensitivity to high-dose androgen therapy and pharmacological inhibition of wild type SPOP. More generally, these results define a distinct class of antagonistic cancer drivers and a blueprint toward their therapeutic exploitation.
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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.