ArticleOncotarget2016
Keratin 18-deficiency results in steatohepatitis and liver tumors in old mice: A model of steatohepatitis-associated liver carcinogenesis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Genome Editing and Fatty Liver.Advances in experimental medicine and biology · 2023Review
- Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research.International journal of molecular sciences · 2022Review
- The application of cytokeratin-18 as a biomarker for drug-induced liver injury.Archives of toxicology · 2021Review
- Revealing the Roles of Keratin 8/18-Associated Signaling Proteins Involved in the Development of Hepatocellular Carcinoma.International journal of molecular sciences · 2021Review
- Article
- Modeling Non-Alcoholic Fatty Liver Disease (NAFLD) Using "Good-Fit" Genome-Editing Tools.Cells · 2020Review
- NAFLD Preclinical Models: More than a Handful, Less of a Concern?Biomedicines · 2020Review
- Xanthohumol Inhibits the Growth of Keratin 18-Overexpressed Esophageal Squamous Cell CarcinomaFrontiers in cell and developmental biology · 2020Article
- Pathophysiology of NAFLD and NASH in Experimental Models: The Role of Food Intake Regulating Peptides.Frontiers in endocrinology · 2020Review
- KRT18 is correlated with the malignant status and acts as an oncogene in colorectal cancer.Bioscience reports · 2019Article
- High Keratin 8/18 Ratio Predicts Aggressive Hepatocellular Cancer Phenotype.Translational oncology · 2019Article
- Keratin 17 Promotes Lung Adenocarcinoma Progression by Enhancing Cell Proliferation and Invasion.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Non-alcoholic fatty liver disease severity is modulated by transglutaminase type 2.Cell death & disease · 2018Article
- The long non-coding RNACell stress · 2017Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Backround: Steatohepatitis (SH)-associated liver carcinogenesis is an increasingly important issue in clinical medicine. SH is morphologically characterized by steatosis, hepatocyte injury, ballooning, hepatocytic cytoplasmic inclusions termed Mallory-Denk bodies (MDBs), inflammation and fibrosis.
results17-20-months-old Krt18-/- and Krt18+/- mice in contrast to wt mice spontaneously developed liver lesions closely resembling the morphological spectrum of human SH as well as liver tumors. The pathologic alterations were more pronounced in Krt18-/- than in Krt18+/- mice. The frequency of liver tumors with male predominance was significantly higher in Krt18-/- compared to age-matched Krt18+/- and wt mice. Krt18-deficient tumors in contrast to wt animals displayed SH features and often pleomorphic morphology. aCGH analysis of tumors revealed chromosomal aberrations in Krt18-/- liver tumors, affecting loci of oncogenes and tumor suppressor genes. MATERIALS AND
methodsLivers of 3-, 6-, 12- and 17-20-months-old aged wild type (wt), Krt18+/- and Krt18-/- (129P2/OlaHsd background) mice were analyzed by light and immunofluorescence microscopy as well as immunohistochemistry. Liver tumors arising in aged mice were analyzed by array comparative genomic hybridization (aCGH).
conclusionsOur findings show that K18 deficiency of hepatocytes leads to steatosis, increasing with age, and finally to SH. K18 deficiency and age promote liver tumor development in mice, frequently on the basis of chromosomal instability, resembling human HCC with stemness features.
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