ArticleOncogenesis2020
EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c.
Article in Oncogenesis, 2020. 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, 27 citations in OpenAlex.
- Exploring the connection between the Mitochondrial DNA and the Circadian Rhythm: Insights into Mitochondrial Biogenesis and its Dynamics.Molecular biology reports · 2025Review
- Observation of PICALM::MLLT10-rearrangement and coincidental EZH2 mutations in a patient with acute myeloid leukemia: A case report and review of the literature.BJC reports · 2025Article
- CircRBM33 competitively binds miR-15a-5p to mediate EZH1 expression to ameliorate sepsis-induced acute lung injury.Clinics (Sao Paulo, Brazil) · 2025Article
- Dual-target EZH2 inhibitor: latest advances in medicinal chemistry.Future medicinal chemistry · 2024Review
- Cathepsin-facilitated invasion of BMI1-high hepatocellular carcinoma cells drives bile duct tumor thrombi formation.Nature communications · 2023Article
- Histone Modifications in NAFLD: Mechanisms and Potential Therapy.International journal of molecular sciences · 2023Review
- Analysis on EZH2: mechanism identification of related CeRNA and its immunoassay in hepatocellular carcinoma.BMC medical genomics · 2023Article
- EZH2 in hepatocellular carcinoma: progression, immunity, and potential targeting therapies.Experimental hematology & oncology · 2023Review
- Hepatitis B Virus Surface Antigen Promotes Stemness of Hepatocellular Carcinoma through Regulating MicroRNA-203a.Journal of clinical and translational hepatology · 2023Article
- Comprehensive competitive endogenous RNA network analysis revealsIranian journal of basic medical sciences · 2022Article
- Upregulation of the ErbB family by EZH2 in hepatocellular carcinoma confers resistance to FGFR inhibitor.Journal of cancer research and clinical oncology · 2021Article
- Tumor Suppressor miRNA in Cancer Cells and the Tumor Microenvironment: Mechanism of Deregulation and Clinical Implications.Frontiers in oncology · 2021Review
- Hepatitis B Virus Promotes Hepatocellular Carcinoma Progression Synergistically With Hepatic Stellate CellsFrontiers in molecular biosciences · 2021Article
- MicroRNA-20a Suppresses Tumor Proliferation and Metastasis in Hepatocellular Carcinoma by Directly Targeting EZH1.Frontiers in oncology · 2021Article
- Single-Cell RNA Sequencing Reveals the Role of Phosphorylation-Related Genes in Hepatocellular Carcinoma Stem Cells.Frontiers in cell and developmental biology · 2021Article
- Mechanisms and Functions of MiR-200 Family in Hepatocellular Carcinoma.OncoTargets and therapy · 2020Review
- Roles of BMI1 in the Initiation, Progression, and Treatment of Hepatocellular Carcinoma.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EZH2, a histone methyltransferase, has been shown to involve in cancer development and progression via epigenetic regulation of tumor suppressor microRNAs, whereas BMI1, a driver of hepatocellular carcinoma (HCC), is a downstream target of these microRNAs. However, it remains unclear whether EZH2 can epigenetically regulate microRNA expression to modulate BMI1-dependent hepatocarcinogenesis. Here, we established that high EZH2 expression correlated with enhanced tumor size, elevated metastasis, increased relapse, and poor prognosis in HCC patients. Further clinical studies revealed that EZH2 overexpression was positively correlated to its gene copy number gain/amplification in HCC. Mechanistically, EZH2 epigenetically suppressed miR-200c expression both in vitro and in vivo, and more importantly, miR-200c post-transcriptionally regulated BMI1 expression by binding to the 3'-UTR region of its mRNA. Furthermore, miR-200c overexpression inhibits the growth of HCC cells in vivo. Silencing miR-200c rescued the tumorigenicity of EZH2-depleted HCC cells, whereas knocking down BMI1 reduced the promoting effect of miR-200c depletion on HCC cell migration. Finally, combination treatment of EZH2 and BMI1 inhibitors further inhibited the viability of HCC cells compared with the cells treated with EZH2 or BMI1 inhibitor alone. Our findings demonstrated that alteration of EZH2 gene copy number status induced BMI1-mediated hepatocarcinogenesis via epigenetically silencing miR-200c, providing novel therapeutic targets for HCC treatment.
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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.