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Aims<\/jats:title>\n                    <jats:p>Hepatoblastoma (HB) is the most common malignant liver tumour in children. Despite improved survival in low\u2010risk 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\u2010driven transcriptomic landscape of HB and identify key mediators of tumour progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Transcriptomic 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\u2010mediated knockdown in\u00a0vitro and in a \u03b2\u2010catenin\/YAP\u2010driven mouse model of HB.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Hypoxia induced broad transcriptional reprogramming in HB cells, including significant upregulation of\n                      <jats:italic>TFF3<\/jats:italic>\n                      , 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\u2010independent growth and cisplatin resistance under both normoxia and hypoxia. Knockdown of murine\n                      <jats:italic>Tff3<\/jats:italic>\n                      suppressed tumour formation and angiogenesis in\u00a0vivo. Transcriptomic and molecular analyses revealed that TFF3 sustains\n                      <jats:italic>C\u2010MYC<\/jats:italic>\n                      expression and modulates mTOR\/GSK3\u03b2 signalling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>TFF3 is a hypoxia\u2010inducible factor that enhances HB cell proliferation, survival and chemoresistance. Its tumour\u2010promoting activity through C\u2010MYC and mTOR pathways identifies TFF3 as a potential therapeutic target and circulating biomarker in hepatoblastoma.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/liv.70592","type":"journal-article","created":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T09:50:11Z","timestamp":1773395411000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Trefoil Factor\u20103 Is a Hypoxia\u2010Triggered Pro\u2010Tumorigenic Factor in Hepatoblastoma"],"prefix":"10.1111","volume":"46","author":[{"given":"Luz A.","family":"Mart\u00ednez\u2010P\u00e9rez","sequence":"first","affiliation":[{"name":"Departamento de Ciencias de la Salud, Centro Universitarios de los Altos Universidad de Guadalajara  Tepatitl\u00e1n M\u00e9xico"},{"name":"Hepatology Laboratory, Solid Tumors Program, CIMA, CCUN University of Navarra  Pamplona Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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