ArticleThe Journal of clinical investigation2018
SPOP mutation drives prostate neoplasia without stabilizing oncogenic transcription factor ERG.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 40 citations in OpenAlex.
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Challenges and opportunities for the diverse substrates of SPOP E3 ubiquitin ligase in cancer.Theranostics · 2025Review
- SPOP point mutations regulate substrate preference and affect its function.Cell death & disease · 2024Article
- Pre-Clinical Models to Study Human Prostate Cancer.Cancers · 2023Review
- Mutation-Attention (MuAt): deep representation learning of somatic mutations for tumour typing and subtyping.Genome medicine · 2023Article
- Race and prostate cancer: genomic landscape.Nature reviews. Urology · 2022Review
- Review
- Prostate Cancer Epigenetic Plasticity and Enhancer Heterogeneity: Molecular Causes, Consequences and Clinical Implications.Advances in experimental medicine and biology · 2022Review
- Dynamic prostate cancer transcriptome analysis delineates the trajectory to disease progression.Nature communications · 2021Article
- Reshaping of the androgen-driven chromatin landscape in normal prostate cells by early cancer drivers and effect on therapeutic sensitivity.Cell reports · 2021Article
- Tumor subtype defines distinct pathways of molecular and clinical progression in primary prostate cancer.The Journal of clinical investigation · 2021Article
- Ubiquitin-Mediated Control of ETS Transcription Factors: Roles in Cancer and Development.International journal of molecular sciences · 2021Review
- Loss of Speckle-Type POZ Protein Promotes Prostate Cancer Cell Migration and Invasion Through Upregulation of MCP-1.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Dual functions of SPOP and ERG dictate androgen therapy responses in prostate cancer.Nature communications · 2021Article
- Cellular and Molecular Progression of Prostate Cancer: Models for Basic and Preclinical Research.Cancers · 2020Review
- The diverse roles of SPOP in prostate cancer and kidney cancer.Nature reviews. Urology · 2020Review
- Development of Prostate Cancer Organoid Culture Models in Basic Medicine and Translational Research.Cancers · 2020Review
- SPOP and cancer: a systematic review.American journal of cancer research · 2020Review
- Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications.Medicines (Basel, Switzerland) · 2019Review
- Constructing and Deconstructing Cancers using Human Pluripotent Stem Cells and Organoids.Cell stem cell · 2019Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Nearly 50% of prostate cancers harbor gene fusions that lead to overexpression of the transcription factor ERG, while a mutually exclusive 10% of prostate cancers harbor recurrent mutations in the gene encoding the E3 ubiquitin ligase SPOP. Recent reports suggest that SPOP acts as a ubiquitin ligase for ERG and propose that ERG stabilization is the oncogenic effector of SPOP mutation. Here, we used human prostate cancer samples and showed that the vast majority of human SPOP-mutant cancers do not express ERG. Comparison of SPOP-mutant and ERG-fusion organoid models showed evidence of divergent, rather than common, transcriptional programs. Furthermore, expression of prostate cancer-associated SPOP mutations in genetically engineered mouse models of SPOP-mutant prostate cancer did not result in the expression of ERG protein in histologically normal prostate glands, high-grade prostatic intraepithelial neoplasia, invasive adenocarcinoma, or prostate organoids. In summary, we found no evidence that ERG is an effector of SPOP mutation in human prostate cancer or mouse models.
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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.