ArticleNature genetics2025
Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis.
Article in Nature genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026Review
- Three-dimensional organoid culture enhances functional maturation of human pluripotent stem cell-derived hepatocytes.Molecular biology reports · 2026Article
- APOBEC2 deficiency disrupts hematopoietic lineage commitment, resulting in emergence of dual identity lymphocytes in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Prox1 maintains taste bud structure via inhibition of apoptosis.Cell and tissue research · 2026Article
- Opening the Flood Gates: Epigenetic Regulators Safeguard Against Rogue Lineage Plasticity in Cholangiocarcinoma.Cellular and molecular gastroenterology and hepatology · 2026Article
- Review
- Review
- Bridging pancreatic and hepatic development: overlapping genes and their role in diabetes.Cellular & molecular biology letters · 2025Review
- PROX1 Expression in Resected Non-Small Cell Lung Cancer: Immunohistochemical Profile and Clinicopathological Correlates.Medical sciences (Basel, Switzerland) · 2025Article
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Authors and funding
29 authors.
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Abstract
Cell fate plasticity enables development, yet unlocked plasticity is a cancer hallmark. While transcription master regulators induce lineage-specific genes to restrict plasticity, it remains unclear whether plasticity is actively suppressed by lineage-specific repressors. Here we computationally predict so-called safeguard repressors for 18 cell types that block phenotypic plasticity lifelong. We validated hepatocyte-specific candidates using reprogramming, revealing that prospero homeobox protein 1 (PROX1) enhanced hepatocyte identity by direct repression of alternative fate master regulators. In mice, Prox1 was required for efficient hepatocyte regeneration after injury and was sufficient to prevent liver tumorigenesis. In line with patient data, Prox1 depletion caused hepatocyte fate loss in vivo and enabled the transition of hepatocellular carcinoma to cholangiocarcinoma. Conversely, overexpression promoted cholangiocarcinoma to hepatocellular carcinoma transdifferentiation. Our findings provide evidence for PROX1 as a hepatocyte-specific safeguard and support a model where cell-type-specific repressors actively suppress plasticity throughout life to safeguard lineage identity and thus prevent disease.
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