ArticleNature communications2021
Hyperpolyploidization of hepatocyte initiates preneoplastic lesion formation in the liver.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 49 citations in OpenAlex.
- Air pollution and hepatocellular carcinoma: Integrated network toxicology, machine learning, molecular docking and multiomics analysis.Oncology letters · 2026Article
- Arid1a deficiency promotes hepatocyte hyperpolyploidy and drives intrahepatic cholangiocarcinoma in mice.Hepatology (Baltimore, Md.) · 2026Article
- Caspase-2 deficiency drives pathogenic liver polyploidy and increases age-associated hepatocellular carcinoma in mice.Science advances · 2026Article
- Cell Fusion-Mediated Induction of Polyploidy, Aneuploidy, and Genomic Instability in Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Aurora kinases signaling in cancer: from molecular perception to targeted therapies.Molecular cancer · 2025Review
- In Silico Network Toxicology, Molecular Docking, and Multi-Level Bioinformatics Reveal Methyl Eugenol-Induced Hepatocellular Carcinoma Mechanisms in Humans.Cancer medicine · 2025Article
- Review
- Paracancerous binuclear hepatocytes assessed by computer program is a novel biomarker for short term recurrence of hepatocellular carcinoma after surgery.Scientific reports · 2025Article
- A triterpenoid (corosolic acid) ameliorated AOM-mediated aberrant crypt foci in rats: modulation of Bax/PCNA, antioxidant and inflammatory mechanisms.Journal of molecular histology · 2024Article
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- The Ploidy State as a Determinant of Hepatocyte Proliferation.Seminars in liver disease · 2023Review
- Histological diagnosis of polyploidy discriminates an aggressive subset of hepatocellular carcinomas with poor prognosis.British journal of cancer · 2023Article
- Mcl-1 deficiency in murine livers leads to nuclear polyploidisation and mitotic errors: Implications for hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2023Article
- Transcriptional-translational conflict is a barrier to cellular transformation and cancer progression.Cancer cell · 2023Article
- Innate Immune Zonation in the Liver: NF-κB (p50) Activation and C-Reactive Protein Expression in Response to Endotoxemia Are Zone Specific.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Effects of Sodium Chromate Exposure on Gene Expression Profiles of Primary Rat Hepatocytes (In Vitro).Biological trace element research · 2023Article
- Single-cell resolved ploidy and chromosomal aberrations in nonalcoholic steatohepatitis-(NASH) induced hepatocellular carcinoma and its precursor lesions.Scientific reports · 2022Article
- Polyploidization of Hepatocytes: Insights into the Pathogenesis of Liver Diseases.Biomolecules & therapeutics · 2022Review
- Implications of Polyploidy and Ploidy Alterations in Hepatocytes in Liver Injuries and Cancers.International journal of molecular sciences · 2022Review
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13 authors at 4 institutions in 5 countries.
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Abstract
Hepatocellular carcinoma (HCC) is the most predominant primary malignancy in the liver. Genotoxic and genetic models have revealed that HCC cells are derived from hepatocytes, but where the critical region for tumor foci emergence is and how this transformation occurs are still unclear. Here, hyperpolyploidization of hepatocytes around the centrilobular (CL) region is demonstrated to be closely linked with the development of HCC cells after diethylnitrosamine treatment. We identify the CL region as a dominant lobule for accumulation of hyperpolyploid hepatocytes and preneoplastic tumor foci formation. We also demonstrate that upregulation of Aurkb plays a critical role in promoting hyperpolyploidization. Increase of AURKB phosphorylation is detected on the midbody during cytokinesis, causing abscission failure and hyperpolyploidization. Pharmacological inhibition of AURKB dramatically reduces nucleus size and tumor foci number surrounding the CL region in diethylnitrosamine-treated liver. Our work reveals an intimate molecular link between pathological hyperpolyploidy of CL hepatocytes and transformation into HCC cells.
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