ArticleJournal of hepatology2016
EpCAM-regulated intramembrane proteolysis induces a cancer stem cell-like gene signature in hepatitis B virus-infected hepatocytes.
Article in Journal of hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Review
- Overcoming colorectal cancer and cancer stem cell resistance with photodynamic therapy: new frontiers in oncology.RSC advances · 2025Review
- Circular RNAs in cancer stem cells: Insights into their roles and mechanisms (Review).International journal of molecular medicine · 2025Review
- RNA Helicase DDX5 in Association With IFI16 and the Polycomb Repressive Complex 2 Silences Transcription of the Hepatitis B Virus by Interferon.Journal of medical virology · 2024Article
- Targeting Hepatic Cancer Stem Cells (CSCs) and Related Drug Resistance by Small Interfering RNA (siRNA).Cell biochemistry and biophysics · 2024Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- NDRG1 facilitates self-renewal of liver cancer stem cells by preventing EpCAM ubiquitination.British journal of cancer · 2023Article
- The regulatory effect of the YY1/miR‑HCC2/BAMBI axis on the stemness of liver cancer cells.International journal of oncology · 2023Article
- Hepatocellular Carcinoma Gene Expression:iLIVER · 2023Review
- Article
- Hepatitis B and Hepatitis C Virus Infection Promote Liver Fibrogenesis through a TGF-β1-Induced OCT4/Nanog Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Hepatitis B Virus Pregenomic RNA Reflecting Viral Replication in Distal Non-tumor Tissues as a Determinant of the Stemness and Recurrence of Hepatocellular Carcinoma.Frontiers in microbiology · 2022Article
- Mechanisms of DNA Methylation in Virus-Host Interaction in Hepatitis B Infection: Pathogenesis and Oncogenetic Properties.International journal of molecular sciences · 2021Review
- The Role of IGF/IGF-1R Signaling in Hepatocellular Carcinomas: Stemness-Related Properties and Drug Resistance.International journal of molecular sciences · 2021Review
- Photodynamic and Photothermal Therapy of Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
- Epigenetic mechanisms in hepatitis B virus-associated hepatocellular carcinoma.Hepatoma research · 2021Article
- Article
- Congenital Tufting Enteropathy: Biology, Pathogenesis and Mechanisms.Journal of clinical medicine · 2020Review
- Genomic Landscape of HCC.Current hepatology reports · 2020Article
- Cancer stemness in hepatocellular carcinoma: mechanisms and translational potential.British journal of cancer · 2020Review
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsHepatocytes in which the hepatitis B virus (HBV) is replicating exhibit loss of the chromatin modifying polycomb repressive complex 2 (PRC2), resulting in re-expression of specific, cellular PRC2-repressed genes. Epithelial cell adhesion molecule (EpCAM) is a PRC2-repressed gene, normally expressed in hepatic progenitors, but re-expressed in hepatic cancer stem cells (hCSCs). Herein, we investigated the functional significance of EpCAM re-expression in HBV-mediated hepatocarcinogenesis.
methodsEmploying molecular approaches (transfections, fluorescence-activated cell sorting, immunoblotting, qRT-PCR), we investigated the role of EpCAM-regulated intramembrane proteolysis (RIP) in HBV replicating cells in vitro, and in liver tumors from HBV X/c-myc mice and chronically HBV infected patients.
resultsEpCAM undergoes RIP in HBV replicating cells, activating canonical Wnt signaling. Transfection of Wnt-responsive plasmid expressing green fluorescent protein (GFP) identified a GFP
conclusionsThe hCSC-like gene signature offers promise as prognostic tool for classifying subtypes of HBV-induced HCCs. Since EpCAM RIP and Wnt signaling drive expression of this hCSC-like signature, inhibition of these pathways can be explored as therapeutic strategy for this subtype of HBV-associated HCCs. LAY SUMMARY: In this study, we provide evidence for a molecular mechanism by which chronic infection by the hepatitis B virus results in the development of poor prognosis liver cancer. Based on this mechanism our results suggest possible therapeutic interventions.
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