ArticleThe American journal of pathology2020
The Hippo Effector Transcriptional Coactivator with PDZ-Binding Motif Cooperates with Oncogenic β-Catenin to Induce Hepatoblastoma Development in Mice and Humans.
Article in The American journal of pathology, 2020. 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 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 52 citations in OpenAlex.
- β-Catenin regulates distinct pathways from YAP and suppresses ONECUT1 to drive hepatoblastoma development in mice and humans.Hepatology (Baltimore, Md.) · 2026Article
- Gas1-Mediated Suppression of Hepatoblastoma Tumorigenesis.The American journal of pathology · 2025Article
- Hepatoblastoma: From Molecular Mechanisms to Therapeutic Strategies.Current oncology (Toronto, Ont.) · 2025Review
- Dynamic YAP expression in the non-parenchymal liver cell compartment controls heterologous cell communication.Cellular and molecular life sciences : CMLS · 2024Article
- FXR Friend-ChIPs in the Enterohepatic System.Seminars in liver disease · 2023Review
- Genome-wide mapping of cancer dependency genes and genetic modifiers of chemotherapy in high-risk hepatoblastoma.Nature communications · 2023Article
- The Hippo Pathway Effectors YAP/TAZ-TEAD Oncoproteins as Emerging Therapeutic Targets in the Tumor Microenvironment.Cancers · 2023Review
- Inhibition of Heat Shock Factor 1 Signaling Decreases Hepatoblastoma Growth via Induction of Apoptosis.The American journal of pathology · 2023Article
- Article
- The Hippo pathway effector TAZ induces intrahepatic cholangiocarcinoma in mice and is ubiquitously activated in the human disease.Journal of experimental & clinical cancer research : CR · 2022Article
- β-Catenin signaling in hepatocellular carcinoma.The Journal of clinical investigation · 2022Review
- TAZ is indispensable for c-MYC-induced hepatocarcinogenesis.Journal of hepatology · 2022Article
- A positive feedback loop of the TAZ/β-catenin axis promotesFrontiers in microbiology · 2022Article
- Increased expression of TAZ and associated upregulation of PD-L1 in cervical cancer.Cancer cell international · 2021Article
- Loss of Apc Cooperates with Activated Oncogenes to Induce Liver Tumor Formation in Mice.The American journal of pathology · 2021Article
- Molecular Mechanisms of Hepatoblastoma.Seminars in liver disease · 2021Article
Corrections and comments
- Erratum issuedCorrection.2020
Authors and funding
17 authors at 9 institutions in 7 countries.
Funding
Abstract
Hepatoblastoma (HB) is the most common pediatric liver tumor. Though Wnt/β-catenin and Hippo cascades are implicated in HB development, studies on crosstalk between β-catenin and Hippo downstream effector transcriptional coactivator with PDZ-binding motif (TAZ) in HB are lacking. Expression levels of TAZ and β-catenin in human HB specimens were assessed by immunohistochemistry. Functional interplay between TAZ and β-catenin was determined by overexpression of an activated form of TAZ (TAZS89A), either alone or combined with an oncogenic form of β-catenin (ΔN90-β-catenin), in mouse liver via hydrodynamic transfection. Activation of TAZ often co-occurred with that of β-catenin in clinical specimens. Although the overexpression of TAZS89A alone did not induce hepatocarcinogenesis, concomitant overexpression of TAZS89A and ΔN90-β-catenin triggered the development of HB lesions exhibiting both epithelial and mesenchymal features. Mechanistically, TAZ/β-catenin-driven HB development required TAZ interaction with transcriptional enhanced associate domain factors. Blockade of the Notch cascade did not inhibit TAZ/β-catenin-dependent HB formation in mice but suppressed the mesenchymal phenotype. Neither Yes-associated protein nor heat shock factor 1 depletion affected HB development in TAZ/β-catenin mice. In human HB cell lines, silencing of TAZ resulted in decreased cell growth, which was further reduced when TAZ knockdown was associated with suppression of either β-catenin or Yes-associated protein. Overall, our study identified TAZ as a crucial oncogene in HB development and progression.
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Registered trials
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