ArticleOncogene2013
DNA damage-induced sustained p53 activation contributes to inflammation-associated hepatocarcinogenesis in rats.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- AI-aided identification of dual-purpose therapeutic targets PRPF19 and MAPK9 in hepatocellular carcinoma and cellular senescence.npj aging · 2025Article
- Inflammation in cancer: therapeutic opportunities from new insights.Molecular cancer · 2025Review
- Glioblastoma Multiforme: Sensitivity to Antimicrobial Peptides LL-37 and PG-1, and Their Combination with Chemotherapy for Predicting the Overall Survival of Patients.Pharmaceutics · 2024Article
- Expression of molecular markers and synergistic anticancer effects of chemotherapy with antimicrobial peptides on glioblastoma cells.Cancer chemotherapy and pharmacology · 2024Article
- Mechanisms ofOpen medicine (Warsaw, Poland) · 2024Article
- SOCS1 Deficiency Promotes Hepatocellular Carcinoma via SOCS3-Dependent CDKN1A Induction and NRF2 Activation.Cancers · 2023Article
- Early warning and diagnosis of liver cancer based on dynamic network biomarker and deep learning.Computational and structural biotechnology journal · 2023Article
- The landscape of aging.Science China. Life sciences · 2022Review
- In Vitro Evaluation of the Cytotoxic Effect ofMolecules (Basel, Switzerland) · 2022Article
- EP300 knockdown reduces cancer stem cell phenotype, tumor growth and metastasis in triple negative breast cancer.BMC cancer · 2020Article
- p53 as a Dichotomous Regulator of Liver Disease: The Dose Makes the Medicine.International journal of molecular sciences · 2018Review
- Diethylnitrosamine Increases Proliferation in Early Stages of Hepatic Carcinogenesis in Insulin-Treated Type 1 Diabetic Mice.BioMed research international · 2018Article
- The matricellular protein CCN1 suppresses hepatocarcinogenesis by inhibiting compensatory proliferation.Oncogene · 2016Article
- p53 amplifies Toll-like receptor 5 response in human primary and cancer cells through interaction with multiple signal transduction pathways.Oncotarget · 2015Article
- Current and emerging biomarkers of cell death in human disease.BioMed research international · 2014Review
- p53 promotes inflammation-associated hepatocarcinogenesis by inducing HMGB1 release.Journal of hepatology · 2013Article
- Absence of a p53 allele delays nitrogen mustard-induced early apoptosis and inflammation of murine skin.Toxicology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The tumor suppressor p53 has an important role in inducing cell-intrinsic responses to DNA damage, including cellular senescence or apoptosis, which act to thwart tumor development. It has been shown, however, that senescent or dying cells are capable of eliciting inflammatory responses, which can have pro-tumorigenic effects. Whether DNA damage-induced p53 activity can contribute to senescence- or apoptosis-associated pro-tumorigenic inflammation is unknown. Recently, we generated a p53 knock-out rat via homologous recombination in rat embryonic stem cells. Here we show that in a rat model of inflammation-associated hepatocarcinogenesis, heterozygous deficiency of p53 resulted in attenuated inflammatory responses and ameliorated hepatic cirrhosis and tumorigenesis. Chronic administration of hepatocarcinogenic compound, diethylnitrosamine, led to persistent DNA damage and sustained induction of p53 protein in the wild-type livers, and much less induction in p53 heterozygous livers. Sustained p53 activation subsequent to DNA damage was accompanied by apoptotic rather than senescent hepatic injury, which gave rise to the hepatic inflammatory responses. In contrast, the non-hepatocarcinogenic agent, carbon tetrachloride, failed to induce p53, and caused a similar degree of chronic hepatic inflammation and cirrhosis in wild type and p53 heterozygous rats. These results suggest that although p53 is usually regarded as a tumor suppressor, its constant activation can promote pro-tumorigenic inflammation, especially in livers exposed to agents that inflict lasting mutagenic DNA damage.
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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.