ArticleOncology reports2014
HBD-2 is downregulated in oral carcinoma cells by DNA hypermethylation, and increased expression of hBD-2 by DNA demethylation and gene transfection inhibits cell proliferation and invasion.
Article in Oncology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- HPV16 E7 inhibits HBD2 expression by down-regulation of ASK1-p38 MAPK pathway in cervical cancer.Virology journal · 2025Article
- Accelerated cognitive aging in chronically infected HIV-1 positive individuals despite effective long-term antiretroviral therapy.Metabolic brain disease · 2024Article
- Multimodal AI/ML for discovering novel biomarkers and predicting disease using multi-omics profiles of patients with cardiovascular diseases.Scientific reports · 2024Article
- Identification of human host factors required for beta-defensin-2 expression in intestinal epithelial cells upon a bacterial challenge.Scientific reports · 2024Article
- Beta-defensin index: A functional biomarker for oral cancer detection.Cell reports. Medicine · 2024Article
- Application Value of Antimicrobial Peptides in Gastrointestinal Tumors.International journal of molecular sciences · 2023Review
- Roles of Antimicrobial Peptides in Gynecological Cancers.International journal of molecular sciences · 2022Review
- Human β-Defensin 2 (HBD-2) Displays Oncolytic Activity but Does Not Affect Tumour Cell Migration.Biomolecules · 2022Article
- Epigenetic Regulation of Host Defense Peptide Synthesis: Synergy Between Histone Deacetylase Inhibitors and DNA/Histone Methyltransferase Inhibitors.Frontiers in immunology · 2022Article
- Defensins: A Double-Edged Sword in Host Immunity.Frontiers in immunology · 2020Review
- Alterations in gene expression and DNA methylation profiles in gastric cancer cells obtained from ascitic fluids collected before and after chemotherapy.Molecular and clinical oncology · 2019Article
- Human Beta Defensins and Cancer: Contradictions and Common Ground.Frontiers in oncology · 2019Review
- Enediyne-activated, EGFR-targeted human β-defensin 1 has therapeutic efficacy against non-small cell lung carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Cell culture models of oral mucosal barriers: A review with a focus on applications, culture conditions and barrier properties.Tissue barriers · 2018Review
- Development of a Cell-Based High-Throughput Screening Assay to Identify Porcine Host Defense Peptide-Inducing Compounds.Journal of immunology research · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human β-defensin-2 (hBD-2) is a type of epithelial antimicrobial peptide. The expression level of hBD-2 mRNA is lower in oral carcinoma cells (OCCs) than in healthy oral epithelium. Yet, it is still unknown how hBD-2 expression is downregulated in OCCs. The present study investigated DNA hypermethylation of hBD-2 in OCCs and the effect of the demethylation and increased expression of hBD-2 on cell proliferation and invasion. Six different types of oral carcinoma cell lines (OSC-19, BSC-OF, SAS, HSC-2, HSC-4 and HSY) and normal oral keratinocytes (NOKs) were used. The expression levels of hBD-2 in all OCCs were significantly lower than that in the NOKs. Treatment with DNA methyltransferase inhibitor, 5-aza-dC, at the concentration of 50 µM significantly induced upregulation of expression of hBD-2 in the OCCs. Using methylation-specific PCR, DNA hypermethylation was observed in all OCCs. These results suggest that DNA hypermethylation is, at least in part, involved in the decreased expression of hBD-2 in OCCs. We examined the effect of 5-aza-dC on the cell proliferation and invasive ability of OCCs. The cell invasion assays showed that the number of OCCs treated with 5-aza-dC on the filters was significantly lower than that of the controls. We examined whether increased expression of hBD-2 generated by gene transfection inhibited the proliferation and invasion of SAS cells. The number of SAS cells exhibiting increased expression of hBD-2 on the filters in the invasion assay were significantly lower on day 7 when compared with the control. hBD-2 may function as a tumor suppressor. Increased expression of hBD-2 induced by demethylation or increased expression generated by gene transfection may be useful therapeutic methods for oral carcinoma.
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