ArticleGastroenterology2011
A mouse model of cholestasis-associated cholangiocarcinoma and transcription factors involved in progression.
Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 128 citations in OpenAlex.
- Association between Helicobacter pylori and Hepatobiliary Cancer: A Meta-analysis and Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2024Pooled it
- Criteria for preclinical models of cholangiocarcinoma: scientific and medical relevance.Nature reviews. Gastroenterology & hepatology · 2023Guideline
- How to efficiently establish animal models of cholangiocarcinoma: challenges and inspiration.Medical review (2021) · 2026Review
- Preclinical mouse models for studying cholangiocarcinoma.Liver research (Beijing, China) · 2026Review
- [Pathology of liver tumours in animal models].Pathologie (Heidelberg, Germany) · 2025Review
- Review: Progress of the NLRP3 inflammasome in tumours and perspectives for cholangiocarcinoma.Cell communication and signaling : CCS · 2025Review
- Secreted AZGP1 induced by 5-FU binds to PD-L1 and promotes apoptosis in cholangiocarcinoma.Molecular medicine (Cambridge, Mass.) · 2025Article
- Pre-diagnostic circulating bile acid concentrations and liver cancer risk: a nested case-control analysis of 12 cohorts.JNCI cancer spectrum · 2025Article
- Hepatic Nuclear Receptors in Cholestasis-to-Cholangiocarcinoma Pathology.The American journal of pathology · 2025Review
- Aurora B facilitates cholangiocarcinoma progression by stabilizing c-Myc.Animal models and experimental medicine · 2024Article
- A DNA/RNA heteroduplex oligonucleotide coupling asparagine depletion restricts FGFR2 fusion-driven intrahepatic cholangiocarcinoma.Molecular therapy. Nucleic acids · 2023Article
- New and Old Key Players in Liver Cancer.International journal of molecular sciences · 2023Review
- Primary Sclerosing Cholangitis-Associated Cholangiocarcinoma: From Pathogenesis to Diagnostic and Surveillance Strategies.Cancers · 2023Review
- A Novel Mouse Model of Intrahepatic Cholangiocarcinoma Induced by Azoxymethane.International journal of molecular sciences · 2023Article
- Tumor Cell-Derived Extracellular Vesicles Promote the Growth, Metastasis and Chemoresistance in Cholangiocarcinoma by Delivering microRNA-210 to Downregulate RECK.Molecular biotechnology · 2023Article
- Review
- The role of LIN28B in tumor progression and metastasis in solid tumor entities.Oncology research · 2023Review
- Selecting an Appropriate Experimental Animal Model for Cholangiocarcinoma Research.Journal of clinical and translational hepatology · 2022Review
- The LIN28B/TGF-β/TGFBI feedback loop promotes cell migration and tumour initiation potential in cholangiocarcinoma.Cancer gene therapy · 2022Article
- LIN28A: A multifunctional versatile molecule with future therapeutic potential.World journal of biological chemistry · 2022Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
BACKGROUND &
aimsCholestasis contributes to hepatocellular injury and promotes liver carcinogenesis. We created a mouse model of chronic cholestasis to study its effects on progression of cholangiocarcinoma and the oncogenes involved.
methodsTo induce chronic cholestasis, Balb/c mice were given 2 weekly intraperitoneal injections of diethylnitrosamine (DEN); 2 weeks later, some mice also received left and median bile duct ligation (LMBDL) and, then 1 week later, were fed DEN, in corn oil, weekly by oral gavage (DLD). Liver samples were analyzed by immunohistochemical and biochemical assays; expression of Mnt and c-Myc was reduced by injection of small inhibitor RNAs.
resultsChronic cholestasis was induced by DLD and accelerated progression of cholangiocarcinoma, compared with mice given only DEN. Cystic hyperplasias, cystic atypical hyperplasias, cholangiomas, and cholangiocarcinoma developed in the DLD group at weeks 8, 12, 16, and 28, respectively. LMBDL repressed expression of microRNA (miR)-34a and let-7a, up-regulating Lin-28B, hypoxia-inducible factor (HIF)-1α, HIF-2α, and miR-210. Up-regulation of Lin-28B might inhibit let-7a, which is associated with development of cystic hyperplasias, cystic atypical hyperplasias, cholangiomas, and cholangiocarcinoma. Knockdown of c-Myc reduced progression of cholangiocarcinoma, whereas knockdown of Mnt accelerated its progression. Down-regulation of miR-34a expression might up-regulate c-Myc. The up-regulation of miR-210 via HIF-2α was involved in down-regulation of Mnt. Activation of the miR-34a-c-Myc and HIF-2α-miR-210-Mnt pathways caused c-Myc to bind the E-box element of cyclin D1, instead of Mnt, resulting in cyclin D1 up-regulation.
conclusionsDLD induction of chronic cholestasis accelerated progression of cholangiocarcinoma, which is mediated by down-regulation of miR-34a, up-regulation miR-210, and replacement of Mnt by c-Myc in binding to cyclin D1.
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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.