ReviewJournal of translational medicine2025
The impact of dysregulation SUMOylation on prostate cancer.
Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Integrated multi-omics and machine learning highlight PTM-related genes as potential biomarkers in endometrial cancer.Translational oncology · 2026Article
- Multi-omics analysis reveals PIAS family gene dysregulation as a driver of head and neck squamous cell carcinoma (HNSC) progression and therapeutic vulnerability.Discover oncology · 2025Article
- Editorial: Post-translational modifications in human cancer: pharmacological insights and therapeutic opportunities.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Prostate cancer (PCa) remains one of the most common malignancies in men, with its development and progression being governed by complex molecular pathways. SUMOylation, a post-translational modification (PTM) that involves the covalent attachment of small ubiquitin-like modifier (SUMO) proteins to target substrates, has emerged as a critical regulator of various cellular processes such as transcription, DNA repair, cell cycle progression, and apoptosis. Emerging evidence reveals that abnormal SUMOylation may contribute to PCa pathogenesis, and notably, SUMO-associated enzymes are commonly dysregulated in PCa. This review explores the mechanisms by which SUMOylation is implicated in the regulation of key pathways, and summary aberrant expression of SUMO-related enzymes or SUMOylation sites mutations of substrtes in PCa, as well as the therapeutic implications of targeting the SUMO-related enzymes in PCa treatment.
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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.