ArticleRedox biology2022
Nrf2 induces malignant transformation of hepatic progenitor cells by inducing β-catenin expression.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Research progress on the protective effect and oxidative stress mechanism of rutin against liver injury (Review).Molecular medicine reports · 2026Review
- Lactylation of β-catenin promotes non-small cell lung cancer by inhibiting ferroptosis through TCF4-mediated GPX4 transcription.Journal of translational medicine · 2026Article
- Review
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Metabolic and Epigenetic Mechanisms in Hepatoblastoma: Insights into Tumor Biology and Therapeutic Targets.Genes · 2024Review
- Promotion of hepatocellular carcinoma stemness and progression by abnormal spindle-like microcephaly-associated protein via the Wnt/β-catenin pathway.Journal of gastrointestinal oncology · 2024Article
- AVERON notebook to discover actionable cancer vulnerabilities enabled by neomorph protein-protein interactions.iScience · 2024Article
- Hypoxia, oxidative stress, and the interplay of HIFs and NRF2 signaling in cancer.Experimental & molecular medicine · 2024Review
- The Contribution of the Nrf2/ARE System to Mechanotransduction in Musculoskeletal and Periodontal Tissues.International journal of molecular sciences · 2023Review
- Emerging Role of NRF2 Signaling in Cancer Stem Cell Phenotype.Molecules and cells · 2023Review
- Health Benefits of Coffee Consumption for Cancer and Other Diseases and Mechanisms of Action.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Nrf2 signaling pathway prevents cancer initiation, but genetic mutations that activate this pathway are found in various types of cancer. The molecular mechanisms underlying this Janus-headed character are still not understood. Here, we show that sustained Nrf2 activation induces proliferation and dedifferentiation of a Wnt-responsive perivenular hepatic progenitor cell population, transforming them into metastatic cancer cells. The neoplastic lesions display many histological features known from human hepatoblastoma. We describe an Nrf2-induced upregulation of β-catenin expression and its activation as the underlying mechanism for the observed malignant transformation. Thus, we have identified the Nrf2-β-catenin axis promoting proliferation of hepatic stem cells and triggering tumorigenesis. These findings support the concept that different functional levels of Nrf2 control both the protection against various toxins as well as liver regeneration by activating hepatic stem cells. Activation of the hepatic stem cell compartment confers the observation that unbridled Nrf2 activation may trigger tumorigenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.