ArticleCancer research2023
A Pro-Regenerative Environment Triggers Premalignant to Malignant Transformation of Senescent Hepatocytes.
Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Induced Molecular Orientation Transition via Organic-Inorganic Hybrid Networks in Thin-Film Transistor-Based Biosensors.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Isomucronulatol attenuates liver aging by inhibiting GSK-3β acetylation and promoting β-catenin accumulation.Journal of natural medicines · 2026Article
- Redefining senescence through hepatocyte fate changes in liver diseases.Trends in endocrinology and metabolism: TEM · 2026Review
- 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
- Upconversion Photoluminescence to Monitor Local Heat Release During Femtosecond Direct Laser Writing of Bioinks In Situ.Small methods · 2026Article
- Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.Journal of hepatology · 2026Review
- Cell senescence in liver diseases: pathological mechanism and theranostic opportunity.Nature reviews. Gastroenterology & hepatology · 2024Review
- Review
- Comprehensive Analyses and Experiments Confirmed IGFBP5 as a Prognostic Predictor Based on an Aging-genomic Landscape Analysis of Ovarian Cancer.Current cancer drug targets · 2024Article
- Liver Injury and Regeneration: Current Understanding, New Approaches, and Future Perspectives.Cells · 2023Review
- Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unfortunately, available liver cancer treatments are associated with modest survival advantage. The biggest factor improving survival is early detection, but the current understanding of early transformation events is limited. Therefore, we set up a model to study these early events and investigated the relationship of premalignant, senescent hepatocytes, a regenerative environment, and the influence of secreted factors on liver tumorigenesis. Oncogene-induced senescence (OIS) was triggered in a subset of mouse hepatocytes, which under normal conditions, are eliminated by immunosurveillance. Inducing liver damage and regeneration was sufficient to trigger immunosurveillance escape of OIS hepatocytes, resulting in premalignant to malignant transformation and hepatocellular tumor development. Trefoil factor 3 (TFF3) was found to be overexpressed in OIS hepatocytes and in hepatocellular carcinoma. TFF3 deficiency strongly attenuated malignant transformation by increasing insulin-like growth factor binding protein 5 (IGFBP5) expression, which consequently dampened IGF receptor signaling. Furthermore, analysis of precancerous liver tissue validated TFF3 as an early liver cancer biomarker. Altogether, these findings provide mechanistic insights into early transformation and immunosurveillance escape in liver cancer, revealing TFF3 and IGFBP5 to be important players with opposite roles in tumorigenesis. SIGNIFICANCE: Liver damage induces a compensatory regenerative response that can drive premalignant to malignant transformation of senescent hepatocytes.
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