ArticleHepatology (Baltimore, Md.)2026
β-Catenin regulates distinct pathways from YAP and suppresses ONECUT1 to drive hepatoblastoma development in mice and humans.
Article in Hepatology (Baltimore, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Single-nucleus transcriptomic atlas of postnatal camel liver development identifies candidate adaptive features.BMC genomics · 2026Article
- Overexpression of ONECUT1 suppresses hepatoblastoma progression via modulating tumor cell growth and tumor microenvironment.Cell & bioscience · 2026Article
- Targeting mTORC2-dependent AKT/FOXO1/RNF125 signaling exploits a therapeutic vulnerability in c-MET-activated and β-catenin-mutated hepatocellular carcinoma.Hepatology (Baltimore, Md.) · 2025Article
- From preneoplastic lesion to heterogenous tumor: recent insights into hepatoblastoma biology and therapeutic opportunities.Molecular cancer · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
BACKGROUND AND
aimsHepatoblastoma (HB) is the predominant primary malignant liver tumor in childhood. Concomitant Yes-associated protein (YAP) and β-Catenin activation occurs in most HB. However, the signaling pathways distinctively regulated by YAP and β-Catenin protooncogenes in HB remain unexplored. APPROACH AND
resultsWe engineered an inducible HB murine model using hydrodynamic injection to deliver transposon plasmids encoding constitutive YAP and doxycycline (Dox)-inducible ΔN90-β-Catenin(YAP/TRE-β-Catenin). Gene expression patterns in mouse HB lesions were analyzed upon short-term Dox withdrawal, that is, tumors still existed but ΔN90-β-Catenin was turned off. The mice rapidly developed aggressive HB lesions when fed Dox. However, upon Dox withdrawal, HB regressed, although tumors did not completely disappear over a long time. At the molecular level, YAP and β-Catenin were found to regulate distinct gene expression programs in HB. Specifically, YAP controls the Hippo and metabolism-related pathways, whereas β-Catenin modulates immune-related pathways, contributing to immune exclusion in the tumor microenvironment. Furthermore, we identified the transcription factor ONECUT1 as a tumor suppressor gene downregulated by activated β-Catenin in HB. Low ONECUT1 expression also characterizes human HB, and the co-expression of ONECUT1 strongly suppressed YAP/β-Catenin-driven HB formation in the mice. Mechanistically, ONECUT1 functions downstream of activated β-Catenin and negatively regulates tumor cell glycolysis.
conclusionsWe show that suppressing activated β-Catenin could hamper HB progression in vivo by affecting pathways distinct from those regulated by YAP in HB. The inhibition of ONECUT1 expression by β-Catenin might represent a critical molecular event leading to HB formation.
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.