ArticleScientific reports2018
Delta-like 3 is silenced by HBx via histone acetylation in HBV-associated HCCs.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Hepatitis B virus promotes hepatocellular carcinoma progression by disrupting NSUN2/YBX1-mediated mVirologica Sinica · 2026Article
- Targeting DLL3: Innovative Strategies for Tumor Treatment.Pharmaceutics · 2025Review
- Hepatitis B virus X protein and TGF-β: partners in the carcinogenic journey of hepatocellular carcinoma.Frontiers in oncology · 2024Review
- Article
- Hepatitis B virus X protein mediated epigenetic alterations in the pathogenesis of hepatocellular carcinoma.Hepatology international · 2022Review
- Methylation-driven gene DLL3 is a potential prognostic biomarker in ocular melanoma correlating with metastasis.Frontiers in oncology · 2022Article
- Are Humanized Mouse Models Useful for Basic Research of Hepatocarcinogenesis through Chronic Hepatitis B Virus Infection?Viruses · 2021Review
- Delta-like canonical Notch ligand 3 as a potential therapeutic target in malignancies: A brief overview.Cancer science · 2021Review
- Host Epigenetic Alterations and Hepatitis B Virus-Associated Hepatocellular Carcinoma.Journal of clinical medicine · 2021Review
- Identification of potential key genes and pathways in hepatitis B virus-associated hepatocellular carcinoma by bioinformatics analyses.Oncology letters · 2020Article
- The Role of DLLs in Cancer: A Novel Therapeutic Target.OncoTargets and therapy · 2020Review
- Delta-like 3 localizes to neuroendocrine cells and plays a pivotal role in gastrointestinal neuroendocrine malignancy.Cancer science · 2019Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a common malignant tumor with poor prognosis. We previously showed that expression of Delta-like 3 (DLL3), a member of the family of Delta/Serrate/Lag2 ligands for the Notch receptor, is silenced by aberrant DNA methylation and that overexpression of DLL3 in an HCC cell line induces cellular apoptosis. However, how DLL3 expression is regulated during hepatocarcinogenesis is still unclear. Here, we show that silencing of DLL3 during hepatocarcinogenesis is closely related to viral infection, especially hepatitis B virus (HBV) infection (p = 0.005). HepG2.2.15 cells, which are stably transformed with the HBV genome, showed lower DLL3 expression than the parent cell line, HepG2 cells. Treatment with Hepatitis B virus X protein (HBx) small interfering RNA upregulated DLL3 expression in HepG2.2.15 cells, and overexpression of HBx in HepG2 cells downregulated DLL3 expression. Treatment of cells with a histone deacetylase inhibitor induced DLL3 expression in HepG2.2.15 cells. These data suggest that DLL3 expression is silenced during hepatocarcinogenesis in association with HBV infection via an epigenetic mechanism.
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