ArticleScience advances2021
Autophagy suppresses the formation of hepatocyte-derived cancer-initiating ductular progenitor cells in the liver.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Obesity and Cancer: From Systemic Metabolic Reprogramming to Immunotherapy Paradox.Metabolites · 2026Review
- Development of a CT radiomics and clinical feature combined model for predicting early recurrence of surgical resected hepatocellular carcinoma.Scientific reports · 2026Article
- Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Attack cancer: Through autophagic modulations as suppressor or promoter.World journal of clinical oncology · 2025Review
- The potential role of hydrogen sulfide-autophagy axis in diseases.Journal of physiology and biochemistry · 2025Review
- 5'-Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation-Mediated PAK2 Upregulation to Promote Cadmium-Induced Breast Cancer Progression by Impairing Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Bioinformatics analysis identifiesTranslational cancer research · 2025Article
- KEAP1 retention in phase-separated p62 bodies drives liver damage under autophagy-deficient conditions.EMBO reports · 2025Article
- Ferroptosis and pyroptosis are connected through autophagy: a new perspective of overcoming drug resistance.Molecular cancer · 2025Review
- Crosstalk between ferroptosis and autophagy: broaden horizons of cancer therapy.Journal of translational medicine · 2025Review
- Autophagy as a potential therapeutic target in regulating improper cellular proliferation.Frontiers in pharmacology · 2025Review
- Nanomaterial-Based Autophagy Modulation: Multiple Weapons to Inflame Immune Systems and the Tumor Microenvironment.Biomaterials research · 2025Review
- Review
- RGS20 promotes non-small cell lung carcinoma proliferation via autophagy activation and inhibition of the PKA-Hippo signaling pathway.Cancer cell international · 2024Article
- Unraveling the complexities of fibrosis and ductular reaction in liver disease: pathogenesis, mechanisms, and therapeutic insights.American journal of physiology. Cell physiology · 2024Review
- New and Old Key Players in Liver Cancer.International journal of molecular sciences · 2023Review
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Autophagy and autophagy-related pathways in cancer.Nature reviews. Molecular cell biology · 2023Review
- Ductular reaction in non-alcoholic fatty liver disease: When Macbeth is perverted.World journal of hepatology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Hepatocellular carcinoma (HCC) is driven by repeated rounds of inflammation, leading to fibrosis, cirrhosis, and, ultimately, cancer. A critical step in HCC formation is the transition from fibrosis to cirrhosis, which is associated with a change in the liver parenchyma called ductular reaction. Here, we report a genetically engineered mouse model of HCC driven by loss of macroautophagy and hemizygosity of phosphatase and tensin homolog, which develops HCC involving ductular reaction. We show through lineage tracing that, following loss of autophagy, mature hepatocytes dedifferentiate into biliary-like liver progenitor cells (ductular reaction), giving rise to HCC. Furthermore, this change is associated with deregulation of yes-associated protein and transcriptional coactivator with PDZ-binding motif transcription factors, and the combined, but not individual, deletion of these factors completely reverses the dedifferentiation capacity and tumorigenesis. These findings therefore increase our understanding of the cell of origin of HCC development and highlight new potential points for therapeutic intervention.
Identifiers
What OpenQuestion holds
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.