ArticleEMBO reports2020
PIDDosome-induced p53-dependent ploidy restriction facilitates hepatocarcinogenesis.
Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Comparative insights into the apoptosome, inflammasomes and PIDDosome.Nature reviews. Immunology · 2026Review
- FOXM1 inhibition primes terminal differentiation of human iPSC-derived hepatocytes.Cell death discovery · 2026Article
- Reciprocal compensation of caspase-2 and p53 regulates the DNA damage response in HCT116 colon cancer cells.The Journal of biological chemistry · 2026Article
- PARP4 ADP-ribosylates PIDD1 to complete a phospho/SUMO/PAR-ylation cascade that orchestrates PIDDosome assembly.Science advances · 2026Article
- Caspase-2 deficiency drives pathogenic liver polyploidy and increases age-associated hepatocellular carcinoma in mice.Science advances · 2026Article
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- Metronidazole induces genotoxicity, hepato- and nephrotoxicity by triggering DNA fragmentation in Swiss albino mice (Balb/c).Scientific reports · 2025Article
- Centriole structural integrity defects are a crucial feature of hydrolethalus syndrome.The Journal of cell biology · 2025Article
- Paracancerous binuclear hepatocytes assessed by computer program is a novel biomarker for short term recurrence of hepatocellular carcinoma after surgery.Scientific reports · 2025Article
- Stepwise phosphorylation and SUMOylation of PIDD1 drive PIDDosome assembly in response to DNA repair failure.Nature communications · 2024Article
- Binucleated human hepatocytes arise through late cytokinetic regression during endomitosis M phase.The Journal of cell biology · 2024Article
- Chronic spindle assembly checkpoint activation causes myelosuppression and gastrointestinal atrophy.EMBO reports · 2024Article
- The Ploidy State as a Determinant of Hepatocyte Proliferation.Seminars in liver disease · 2023Review
- Extra centrosomes induce PIDD1-mediated inflammation and immunosurveillance.The EMBO journal · 2023Article
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Article
- Tumor cell density dependent IL-8 secretion induces the fluctuation of tregs/CD8 + T cells infiltration in hepatocellular carcinoma: one prompt for the existence of density checkpoint.Journal of translational medicine · 2023Article
- Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023Review
- IL6 supports long-term expansion of hepatocytes in vitro.Nature communications · 2022Article
- Centriole signaling restricts hepatocyte ploidy to maintain liver integrity.Genes & development · 2022Article
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20 authors at 8 institutions in 3 countries.
Funding
Abstract
Polyploidization frequently precedes tumorigenesis but also occurs during normal development in several tissues. Hepatocyte ploidy is controlled by the PIDDosome during development and regeneration. This multi-protein complex is activated by supernumerary centrosomes to induce p53 and restrict proliferation of polyploid cells, otherwise prone for chromosomal instability. PIDDosome deficiency in the liver results in drastically increased polyploidy. To investigate PIDDosome-induced p53-activation in the pathogenesis of liver cancer, we chemically induced hepatocellular carcinoma (HCC) in mice. Strikingly, PIDDosome deficiency reduced tumor number and burden, despite the inability to activate p53 in polyploid cells. Liver tumors arise primarily from cells with low ploidy, indicating an intrinsic pro-tumorigenic effect of PIDDosome-mediated ploidy restriction. These data suggest that hyperpolyploidization caused by PIDDosome deficiency protects from HCC. Moreover, high tumor cell density, as a surrogate marker of low ploidy, predicts poor survival of HCC patients receiving liver transplantation. Together, we show that the PIDDosome is a potential therapeutic target to manipulate hepatocyte polyploidization for HCC prevention and that tumor cell density may serve as a novel prognostic marker for recurrence-free survival in HCC patients.
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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.