ReviewMolecular biology reports2026
UHRF1 as an epigenetic therapeutic target in Cancer.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UHRF1 (ubiquitin-like with PHD and RING finger domains 1) is a multi-domain epigenetic regulator that integrates DNA methylation, histone modification, and ubiquitin signaling. Its overexpression is consistently observed across diverse cancers, where it silences tumor suppressor genes, stabilizes oncogenic proteins, and rewires metabolic and stress pathways, thereby driving tumor progression and therapy resistance. Targeting UHRF1 offers a domain-specific and context-dependent strategy distinct from global demethylation, reducing off-target toxicity and providing a refined therapeutic window. Natural compounds such as flavonoids, berberine, and thymoquinone, as well as synthetic inhibitors of reader domains, proteasomal degraders, and RNA-based approaches, have demonstrated potential to disrupt UHRF1 function. UHRF1 inhibition may also synergize with DNMT or HDAC inhibitors, immune checkpoint blockade, and ferroptosis inducers. Current evidence supports UHRF1 as both a biomarker and a promising druggable target for next-generation epigenetic cancer therapies.
Indexed as
Identifiers
41774300What 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.