ArticleLiver international : official journal of the International Association for the Study of the Liver2026
Trefoil Factor-3 Is a Hypoxia-Triggered Pro-Tumorigenic Factor in Hepatoblastoma.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Trefoil Factor-3 Is a Hypoxia-Triggered Pro-Tumorigenic Factor in Hepatoblastoma.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
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26 authors.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsHepatoblastoma (HB) is the most common malignant liver tumour in children. Despite improved survival in low-risk disease, outcomes for advanced or relapsed HB remain poor, emphasising the need for new therapeutic targets. Hypoxia, a hallmark of aggressive tumours, has recently been implicated in HB pathogenesis, but the molecular mechanisms involved are unclear. This study aimed to characterise the hypoxia-driven transcriptomic landscape of HB and identify key mediators of tumour progression.
methodsTranscriptomic analyses of HB cell lines cultured under normoxic and hypoxic conditions were combined with bioinformatic interrogation of public HB datasets, immunohistochemistry of human and murine tumours and plasma ELISA assays. Functional roles of trefoil factor 3 (TFF3) were evaluated through overexpression and shRNA-mediated knockdown in vitro and in a β-catenin/YAP-driven mouse model of HB.
resultsHypoxia induced broad transcriptional reprogramming in HB cells, including significant upregulation of TFF3, a secreted oncogenic peptide. TFF3 expression was elevated in HB tissues and plasma, and colocalized with hypoxia marker carbonic anhydrase 9 (CA9). TFF3 promoted proliferation, anchorage-independent growth and cisplatin resistance under both normoxia and hypoxia. Knockdown of murine Tff3 suppressed tumour formation and angiogenesis in vivo. Transcriptomic and molecular analyses revealed that TFF3 sustains C-MYC expression and modulates mTOR/GSK3β signalling.
conclusionsTFF3 is a hypoxia-inducible factor that enhances HB cell proliferation, survival and chemoresistance. Its tumour-promoting activity through C-MYC and mTOR pathways identifies TFF3 as a potential therapeutic target and circulating biomarker in hepatoblastoma.
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