ReviewThe FEBS journal2019
The ubiquitin ligase adaptor SPOP in cancer.
Review in The FEBS journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 73 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Large-scale quaternary structural transitions underlie gain of function of SPOP cancer mutations.Molecular cell · 2026Article
- Nanobody-based bioPROTAC for viral protein degradation provides an antiviral strategy for porcine arterivirus.Journal of nanobiotechnology · 2026Article
- The Clinical Significance of SPOP Upregulation and Nuclear Accumulation in Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- SPOP-dependent destabilization of SYT12 in a GSK-3β-dependent manner in papillary thyroid cancer cells.Clinical and experimental medicine · 2025Article
- The equilibrium between two quaternary assembly states determines the activity of SPOP and its cancer mutants.bioRxiv : the preprint server for biology · 2025Article
- Cul3 substrate adaptor SPOP targets Nup153 for degradation.Molecular biology of the cell · 2025Article
- Synthesis and Biological Evaluation of β-Lactam Derivatives Targeting Speckle-Type POZ Protein (SPOP).ACS medicinal chemistry letters · 2024Article
- A genetic screen identifies BEND3 as a regulator of bivalent gene expression and global DNA methylation.Nucleic acids research · 2023Article
- Review
- Article
- Overexpression of SERPINA3 suppresses tumor progression by modulating SPOP/NF‑κB in lung cancer.International journal of oncology · 2023Article
- Interrogating bromodomain inhibitor resistance in KMT2A-rearranged leukemia through combinatorial CRISPR screens.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Phase separation in cancer at a glance.Journal of translational medicine · 2023Review
- Higher-order SPOP assembly reveals a basis for cancer mutant dysregulation.Molecular cell · 2023Article
- Phase Separation in Biology and Disease; Current Perspectives and Open Questions.Journal of molecular biology · 2023Article
- Article
- B7-H6 enhances F-actin rearrangement by targeting c-MYC activation to promote medulloblastoma migration and invasion.Medical oncology (Northwood, London, England) · 2023Article
- SPOP loss of function protects against tauopathy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Speckle-type POZ protein could play a potential inhibitory role in human renal cell carcinoma.BMC cancer · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The dysregulation of ubiquitin-mediated proteasomal degradation has emerged as an important mechanism of pathogenesis in several cancers. The speckle-type POZ protein (SPOP) functions as a substrate adaptor for the cullin3-RING ubiquitin ligase and controls the cellular persistence of a diverse array of protein substrates in hormone signalling, epigenetic control and cell cycle regulation, to name a few. Mutations in SPOP and the resulting dysregulation of this proteostatic pathway play causative roles in the pathogenesis of prostate and endometrial cancers, whereas overexpression and mislocalization are associated with kidney cancer. Understanding the molecular mechanism of the normal function of SPOP as well as the cause of SPOP-mediated oncogenesis is thus critical for eventual therapeutic targeting of SPOP and other related pathways. Here, we will review SPOP structure, function and the molecular mechanism of how this function is achieved. We will then review how mutations and protein mislocalization contribute to cancer pathogenesis and will provide a perspective on how SPOP may be targeted therapeutically.
Indexed as
Identifiers
What OpenQuestion holds
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.