ArticleThe American journal of pathology2019
β-Catenin and Yes-Associated Protein 1 Cooperate in Hepatoblastoma Pathogenesis.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Bibliometric and clinical trial landscape of hepatoblastoma (2000-2024): a multi-database analysis of global research.Frontiers in oncology · 2026Pooled it
- Review
- β-Catenin-Cohesin Ring-CEGRs/ALCDs Axis Activation Contributes to the Development of Hepatoblastoma and Fibrolamellar HCC.Molecular cancer research : MCR · 2025Article
- Derivation of Genetically Defined Murine Hepatoblastoma Cell Lines with Angiogenic Potential.Cancers · 2025Article
- From preneoplastic lesion to heterogenous tumor: recent insights into hepatoblastoma biology and therapeutic opportunities.Molecular cancer · 2025Review
- Gas1-Mediated Suppression of Hepatoblastoma Tumorigenesis.The American journal of pathology · 2025Article
- Insights into the mechanisms of angiogenesis in hepatoblastoma.Frontiers in cell and developmental biology · 2025Review
- Wnt/β-Catenin Signaling in Liver Pathobiology.Annual review of pathology · 2025Review
- Targeting the Hippo/YAP1 signaling pathway in hepatocellular carcinoma: From mechanisms to therapeutic drugs (Review).International journal of oncology · 2024Review
- Genome-wide mapping of cancer dependency genes and genetic modifiers of chemotherapy in high-risk hepatoblastoma.Nature communications · 2023Article
- Inhibition of Heat Shock Factor 1 Signaling Decreases Hepatoblastoma Growth via Induction of Apoptosis.The American journal of pathology · 2023Article
- Article
- Hepatocyte-Specific Deletion of Yes-Associated Protein Improves Recovery From Acetaminophen-Induced Acute Liver Injury.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Hepatoblastoma: glutamine depletion hinders cell viability in the embryonal subtype but high GLUL expression is associated with better overall survival.Journal of cancer research and clinical oncology · 2021Article
- Olaparib Inhibits Tumor Growth of Hepatoblastoma in Patient-Derived Xenograft Models.Hepatology (Baltimore, Md.) · 2021Article
- Scaffolding Protein IQGAP1 Is Dispensable, but Its Overexpression Promotes Hepatocellular Carcinoma via YAP1 Signaling.Molecular and cellular biology · 2021Article
- Glutamine Synthetase as a Therapeutic Target for Cancer Treatment.International journal of molecular sciences · 2021Review
- Article
- Help for Sick Kids: New Insights Into Hepatoblastoma.Cellular and molecular gastroenterology and hepatology · 2021Article
- Mutations and Copy Number Abnormalities of Hippo Pathway Components in Human Cancers.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
- Erratum issuedCorrection.2019
Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
Abstract
Hepatoblastoma (HB), the most common pediatric primary liver neoplasm, shows nuclear localization of β-catenin and yes-associated protein 1 (YAP1) in almost 80% of the cases. Co-expression of constitutively active S127A-YAP1 and ΔN90 deletion-mutant β-catenin (YAP1-ΔN90-β-catenin) causes HB in mice. Because heterogeneity in downstream signaling is being identified owing to mutational differences even in the β-catenin gene alone, we investigated if co-expression of point mutants of β-catenin (S33Y or S45Y) with S127A-YAP1 led to similar tumors as YAP1-ΔN90-β-catenin. Co-expression of S33Y/S45Y-β-catenin and S127A-YAP1 led to activation of Yap and Wnt signaling and development of HB, with 100% mortality by 13 to 14 weeks. Co-expression with YAP1-S45Y/S33Y-β-catenin of the dominant-negative T-cell factor 4 or dominant-negative transcriptional enhanced associate domain 2, the respective surrogate transcription factors, prevented HB development. Although histologically similar, HB in YAP1-S45Y/S33Y-β-catenin, unlike YAP1-ΔN90-β-catenin HB, was glutamine synthetase (GS) positive. However, both ΔN90-β-catenin and point-mutant β-catenin comparably induced GS-luciferase reporter in vitro. Finally, using a previously reported 16-gene signature, it was shown that YAP1-ΔN90-β-catenin HB tumors exhibited genetic similarities with more proliferative, less differentiated, GS-negative HB patient tumors, whereas YAP1-S33Y/S45Y-β-catenin HB exhibited heterogeneity and clustered with both well-differentiated GS-positive and proliferative GS-negative patient tumors. Thus, we demonstrate that β-catenin point mutants can also collaborate with YAP1 in HB development, albeit with a distinct molecular profile from the deletion mutant, which may have implications in both biology and therapy.
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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.