ArticleOncotarget2017
MicroRNA deregulation in nonalcoholic steatohepatitis-associated liver carcinogenesis.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Circulating miR-122-5p, miR-151a-3p, miR-126-5p and miR-21-5p as potential predictive biomarkers for Metabolic Dysfunction-Associated Steatotic Liver Disease assessment.Journal of physiology and biochemistry · 2025Article
- A Critical Review on microRNAs as Prognostic Biomarkers in Laryngeal Carcinoma.International journal of molecular sciences · 2024Review
- Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC.International journal of molecular sciences · 2024Review
- Article
- Deletion of platelet-derived growth factor receptor β suppresses tumorigenesis in metabolic dysfunction-associated steatohepatitis (MASH) mice with diabetes.Scientific reports · 2024Article
- Article
- Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2023Review
- Adipose-derived mesenchymal stem cell-secreted extracellular vesicles alleviate non-alcoholic fatty liver diseaseAdipocyte · 2022Article
- The Implications of Noncoding RNAs in the Evolution and Progression of Nonalcoholic Fatty Liver Disease (NAFLD)-Related HCC.International journal of molecular sciences · 2022Review
- Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis.Cellular and molecular life sciences : CMLS · 2022Article
- The Pathogenesis of HCC Driven by NASH and the Preventive and Therapeutic Effects of Natural Products.Frontiers in pharmacology · 2022Review
- Article
- Exosomal MicroRNAs as Potential Biomarkers of Hepatic Injury and Kidney Disease in Glycogen Storage Disease Type Ia Patients.International journal of molecular sciences · 2021Article
- Hepatocellular Carcinoma in Non-Alcoholic Fatty Liver Disease: From Epidemiology to Diagnostic Approach.Cancers · 2021Review
- In Vivo and In Vitro Models of Hepatocellular Carcinoma: Current Strategies for Translational Modeling.Cancers · 2021Review
- The relationship between polyphenols and miRNAs: A novel therapeutic strategy for metabolic associated fatty liver disease.Hepatology forum · 2021Review
- Exosomes secreted by palmitic acid-treated hepatocytes promote LX-2 cell activation by transferring miRNA-107.Cell death discovery · 2021Article
- Emerging roles and mechanisms of microRNA‑222‑3p in human cancer (Review).International journal of oncology · 2021Review
- Xylo-Oligosaccharides in Prevention of Hepatic Steatosis and Adipose Tissue Inflammation: Associating Taxonomic and Metabolomic Patterns in Fecal Microbiomes with Biclustering.International journal of environmental research and public health · 2021Article
- Metabolic disease as a risk of hepatocellular carcinoma.Clinical and molecular hepatology · 2021Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the fastest-rising cause of cancer-related death in the United States. Recent epidemiological studies have identified nonalcoholic steatohepatitis (NASH), a progressive form of nonalcoholic fatty liver disease (NAFLD), as a major risk factor for HCC. Elucidating the underlying mechanisms associated with the development of NASH-derived HCC is critical for identifying early biomarkers for the progression of the disease and for treatment and prevention. In the present study, using liver samples from C57BL/6J mice submitted to the Stelic Animal Model (STAM) of NASH-associated liver carcinogenesis, we investigated the role of microRNA (miRNA) alterations in the pathogenesis of NASH-derived HCC. We found substantial alterations in the expression of miRNAs, with the greatest number occurring in full-fledged HCC. Mechanistically, altered miRNA expression was associated with activation of major hepatocarcinogenesis-related pathways, including the TGF-β, Wnt/β-catenin, ERK1/2, mTOR, and EGF signaling. In addition, the over-expression of the miR-221-3p and miR-222-3p and oncogenic miR-106b∼25 cluster was accompanied by the reduced protein levels of their targets, including E2F transcription factor 1 (E2F1), phosphatase and tensin homolog (PTEN), and cyclin-dependent kinase inhibitor 1 (CDKN1A). Importantly, miR-93-5p, miR-221-3p, and miR-222-3p were also significantly over-expressed in human HCC. These findings suggest that aberrant expression of miRNAs may have mechanistic significance in NASH-associated liver carcinogenesis and may serve as an indicator for the development of NASH-derived HCC.
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Registered trials
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